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Sample records for chronic inflammatory marker

  1. Inflammatory Markers in Recent Onset Psychosis and Chronic Schizophrenia

    PubMed Central

    Dickerson, Faith; Stallings, Cassie; Origoni, Andrea; Schroeder, Jennifer; Katsafanas, Emily; Schweinfurth, Lucy; Savage, Christina; Khushalani, Sunil; Yolken, Robert

    2016-01-01

    Background. Immune markers have been associated with schizophrenia, but few studies have examined multiple markers in both recent onset and chronic schizophrenia patients. Methods. The sample of 588 individuals included 79 with recent onset psychosis, 249 with chronic schizophrenia, and 260 controls. A combined inflammation score was calculated by principal components factor analysis of the levels of C-reactive protein, Pentraxin 3, and IgG antibodies to gliadin, casein, and Saccharomyces cerevisiae measured in blood samples. Inflammation scores among groups were compared by multivariate analyses. Results. The chronic schizophrenia group showed significant elevations in the combined inflammation score compared with controls. The recent onset group surprisingly showed a reduction in the combined inflammation score. Consistent with these findings, the chronic schizophrenia group had significantly increased odds of a combined inflammation score greater than the 75th and the 90th percentile of that of the controls. The recent onset group had significantly increased odds of a combined inflammation score less than the 10th and the 25th percentile level of the controls. Conclusions. The recent onset of psychosis may be associated with inherent deficits in innate immunity. Individuals later in the course of disease may have increased levels of innate immunity. The reasons for these changes are not known with certainty but may be related to compensatory increases as the disease progresses. Longitudinal studies are needed to determine the course of immune abnormalities in schizophrenia and their role in the clinical manifestations of the disorder. PMID:26294704

  2. Inflammatory Markers in Recent Onset Psychosis and Chronic Schizophrenia.

    PubMed

    Dickerson, Faith; Stallings, Cassie; Origoni, Andrea; Schroeder, Jennifer; Katsafanas, Emily; Schweinfurth, Lucy; Savage, Christina; Khushalani, Sunil; Yolken, Robert

    2016-01-01

    Immune markers have been associated with schizophrenia, but few studies have examined multiple markers in both recent onset and chronic schizophrenia patients. The sample of 588 individuals included 79 with recent onset psychosis, 249 with chronic schizophrenia, and 260 controls. A combined inflammation score was calculated by principal components factor analysis of the levels of C-reactive protein, Pentraxin 3, and IgG antibodies to gliadin, casein, and Saccharomyces cerevisiae measured in blood samples. Inflammation scores among groups were compared by multivariate analyses. The chronic schizophrenia group showed significant elevations in the combined inflammation score compared with controls. The recent onset group surprisingly showed a reduction in the combined inflammation score. Consistent with these findings, the chronic schizophrenia group had significantly increased odds of a combined inflammation score greater than the 75th and the 90th percentile of that of the controls. The recent onset group had significantly increased odds of a combined inflammation score less than the 10th and the 25th percentile level of the controls. The recent onset of psychosis may be associated with inherent deficits in innate immunity. Individuals later in the course of disease may have increased levels of innate immunity. The reasons for these changes are not known with certainty but may be related to compensatory increases as the disease progresses. Longitudinal studies are needed to determine the course of immune abnormalities in schizophrenia and their role in the clinical manifestations of the disorder. © The Author 2015. Published by Oxford University Press on behalf of the Maryland Psychiatric Research Center. All rights reserved. For permissions, please email: journals.permissions@oup.com.

  3. Impact of Ivabradine on Inflammatory Markers in Chronic Heart Failure

    PubMed Central

    Kretzschmar, Daniel; Pistulli, Rudin; Schulze, P. Christian; Stumpf, Christian; Yilmaz, Atilla

    2016-01-01

    Background. Inflammation plays a crucial role in the progression of chronic heart failure (CHF). Ivabradine is known to reduce the morbidity and mortality of patients with CHF under certain conditions. Beyond the reduction of heart rate, only limited knowledge exists about potential anti-inflammatory effects of ivabradine that might contribute to its benefit in CHF. Thus, the present study aimed to investigate the effect of ivabradine on systemic inflammation. Methods. In the present study, 33 patients with CHF due to dilated, ischemic, and hypertensive cardiomyopathy were treated with ivabradine according to the guidelines of the European Society of Cardiology (ESC). A number of circulating dendritic cells as well as inflammatory mediators were investigated using FACS analysis and ELISA, respectively, before and during ivabradine therapy. Results. Treatment with ivabradine resulted in a significant improvement of CHF symptoms as well as an increase in left ventricular ejection fraction. Moreover, ivabradine treatment led to a significant reduction of TNF-alpha (TNF-α) serum levels and a reconstitution of circulating dendritic cells which are known to be reduced in patients with CHF. Conclusion. We show that treatment with ivabradine in patients with CHF resulted in an improvement of HF symptoms and ejection fraction as well as a normalization of inflammatory mediators. PMID:27822484

  4. Impact of Ivabradine on Inflammatory Markers in Chronic Heart Failure.

    PubMed

    Rohm, Ilonka; Kretzschmar, Daniel; Pistulli, Rudin; Franz, Marcus; Schulze, P Christian; Stumpf, Christian; Yilmaz, Atilla

    2016-01-01

    Background. Inflammation plays a crucial role in the progression of chronic heart failure (CHF). Ivabradine is known to reduce the morbidity and mortality of patients with CHF under certain conditions. Beyond the reduction of heart rate, only limited knowledge exists about potential anti-inflammatory effects of ivabradine that might contribute to its benefit in CHF. Thus, the present study aimed to investigate the effect of ivabradine on systemic inflammation. Methods. In the present study, 33 patients with CHF due to dilated, ischemic, and hypertensive cardiomyopathy were treated with ivabradine according to the guidelines of the European Society of Cardiology (ESC). A number of circulating dendritic cells as well as inflammatory mediators were investigated using FACS analysis and ELISA, respectively, before and during ivabradine therapy. Results. Treatment with ivabradine resulted in a significant improvement of CHF symptoms as well as an increase in left ventricular ejection fraction. Moreover, ivabradine treatment led to a significant reduction of TNF-alpha (TNF-α) serum levels and a reconstitution of circulating dendritic cells which are known to be reduced in patients with CHF. Conclusion. We show that treatment with ivabradine in patients with CHF resulted in an improvement of HF symptoms and ejection fraction as well as a normalization of inflammatory mediators.

  5. Immunomodulation of inflammatory leukocyte markers during intravenous immunoglobulin treatment associated with clinical efficacy in chronic inflammatory demyelinating polyradiculoneuropathy.

    PubMed

    Dyer, Wayne B; Tan, Joanne C G; Day, Timothy; Kiers, Lynette; Kiernan, Matthew C; Yiannikas, Con; Reddel, Stephen; Ng, Karl; Mondy, Phillip; Dennington, Peta M; Dean, Melinda M; Trist, Halina M; Dos Remedios, Cristobal; Hogarth, P Mark; Vucic, Steve; Irving, David O

    2016-10-01

    The objective of the study was to profile leukocyte markers modulated during intravenous immunoglobulin (IVIg) treatment, and to identify markers and immune pathways associated with clinical efficacy of IVIg for chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) with potential for monitoring treatment efficacy. Response to IVIg treatment in newly diagnosed IVIg-naïve and established IVIg-experienced patients was assessed by changes in expression of inflammatory leukocyte markers by flow cytometry. The adjusted INCAT disability and Medical Research Council sum scores defined clinical response. Intravenous immunoglobulin modulated immunopathogenic pathways associated with inflammatory disease in CIDP. Leukocyte markers of clinical efficacy included reduced CD185(+) follicular helper T cells, increased regulatory markers (CD23 and CD72) on B cells, and reduction in the circulating inflammatory CD16(+) myeloid dendritic cell (mDC) population and concomitant increase in CD62L and CD195 defining a less inflammatory lymphoid homing mDC phenotype. A decline in inflammatory CD16(+) dendritic cells was associated with clinical improvement or stability, and correlated with magnitude of improvement in neurological assessment scores, but did not predict relapse. IVIg also induced a nonspecific improvement in regulatory and reduced inflammatory markers not associated with clinical response. Clinically effective IVIg modulated inflammatory and regulatory pathways associated with ongoing control or resolution of CIDP disease. Some of these markers have potential for monitoring outcome.

  6. Effects of honey supplementation on inflammatory markers among chronic smokers: a randomized controlled trial.

    PubMed

    Ghazali, Wan Syaheedah Wan; Romli, Aminah Che; Mohamed, Mahaneem

    2017-03-28

    Honey has been demonstrated to possess anti-inflammatory property. This is a randomized, controlled, open-label trial to determine the effects of 12-week honey oral supplementation on plasma inflammatory markers such as high sensitive C-reactive protein, interleukin-6 and tumor necrosis factor-α among chronic smokers. A total of 32 non-smokers and 64 chronic smokers from Quit Smoking Clinic and Health Campus, Universiti Sains Malaysia participated in the study. Smokers were then randomized into 2 groups: smokers with honey group that received Malaysian Tualang honey (20 g/day daily for 12 weeks) and smokers without honey group. Blood was obtained from non-smokers and smokers at pre-intervention, and from smokers at post-intervention for measurement of the inflammatory markers. At pre-intervention, smokers had significantly higher high sensitive C-reactive protein than non-smokers. In smokers with honey group, tumor necrosis factor-α was significantly increased while high sensitive C-reactive protein was significantly reduced at post-intervention than at pre-intervention. This study suggests that honey supplementation has opposite effects on tumor necrosis factor-α and high sensitive C-reactive protein indicating the inconclusive effect of honey on inflammation among chronic smokers which needs further study on other inflammatory markers. The Trial has been registered in the Australian New Zealand Clinical Trials Registry: ACTRN12615001236583 . Registered 11 November 2015 (Retrospectively Registered).

  7. Systematic review of anaemia and inflammatory markers in chronic obstructive pulmonary disease.

    PubMed

    Hoepers, Andrea Thives de Carvalho; Menezes, Marcia Margarete; Fröde, Tânia Silvia

    2015-03-01

    This systematic review synthesizes the relevant published articles on the prevalence of anaemia in patients with chronic obstructive pulmonary disease (COPD) and its relationship with inflammatory markers. The upregulation of erythropoietin in anaemia maintains homeostasis. However, anaemic COPD patients do not respond to increased levels of erythropoietin. The increased levels could be an indicator of the peripheral erythropoietin resistance in COPD. Anaemia and inflammation are associated with an increased risk of hospitalization and mortality in these patients. The understanding of anaemia in chronic inflammation is that anaemia is at least partially due to the excessive production of inflammatory cytokines, which can contribute to improvements in the management, prognosis, and survival of patients with COPD and anaemia.

  8. Inflammatory Markers and Procoagulants in Chronic Renal Disease Stages 1-4

    PubMed Central

    Muslimovic, Alma; Rasic, Senija; Tulumovic, Denijal; Hasanspahic, Senad; Rebic, Damir

    2015-01-01

    Introduction: Starting from the point that the chronic kidney disease (CKD) is chronic, inflammatory and hypercoagulable state characterized by an increase in procoagulant and inflammatory markers high cardiovascular morbidity and mortality in these patients could be explained. Aim: The aim of the research was to monitor inflammatory markers and procoagulants in various stages of kidney disease (stage 1-4). Materials and Methods: The research included 120 subjects older than 18 years with CKD stages 1-4 examined and monitored in Clinic of Nephrology, University Clinical Centre Sarajevo over a period of 24 months. The research included determining the following laboratory parameters: serum creatinine, serum albumin, C-reactive protein, leukocytes in the blood, plasma fibrinogen, D-dimer, antithrombin III, coagulation factors VII (FC VII) and coagulation factor VIII (FC VIII). Results: With the progression of kidney disease (CKD stages 1-4), there was a significant increase of inflammatory and procoagulant markers: CRP, fibrinogen and coagulation factor VIII, and an increase in the average values of leukocytes and a reduction in the value of antithrombin III, but without statistical significance. Also, there were no significant differences in the values of D-dimer and coagulation factor VII. Conclusion: The progression of kidney disease is significantly associated with inflammation, which could in the future be useful in prognostic and therapeutic purposes. Connection of CKD with inflammation and proven connection of inflammation with cardiovascular risk indicates the potential value of some biomarkers, which could in the future identify as predictors of outcome and could have the benefit in the early diagnosis and treatment of cardiovascular disease in CKD. PMID:26622082

  9. Serum levels of inflammatory markers in type 2 diabetes patients with chronic periodontitis.

    PubMed

    Longo, Priscila Larcher; Artese, Hilana Paula Carillo; Rabelo, Marianade Sousa; Kawamoto, Dione; Foz, Adriana Moura; Romito, Giuseppe Alexandre; Dib, Sergio Atala; Mayer, Marcia Pinto Alves

    2014-04-01

    Diabetes has been associated with periodontitis, but the mechanisms through which periodontal diseases affect the metabolic control remain unclear. This study aimed to evaluate serum leveis of inflammatory markers, IL-8, IL-6 and monocyte chemoattractant protein 1 (MCP-1), in type 2 diabetic patients in the presence of chronic periodontitis. Forty two individuals were enrolled in this study and assigned to one of five groups: diabetes mellitus with inadequate glycemic control and periodontitis (DMI+P, n = 10), diabetes mellitus with adequate glycemic control and periodontitis (DMA+P, n = 10), diabetes mellitus without periodontitis (DM, n = 10), periodontitis without diabetes (P, n=6), and neither diabetes nor periodontitis (H, n = 6). Periodontal clinical examination included visible plaque index (PL), gingival bleeding index (GB), probing depth (PD), attachment level (AL) and bleeding on probing (BP). Glycemic control was evaluated by serum concentration of glycated hemoglobin (HbAlc). Inflammatory serum markers IL-8, IL-6 and (MCP-1) were measured by ELISA. DMI+P and DMA+P groups presented higher PD (p=0.025) and AL (p=0.003) values when compared to the P group. There were no significant differences among groups for IL-6, IL-8 and MCP-1 serum levels. Although periodontitis was more severe in diabetic patients, the serum levels of the investigated inflammatory markers did not differ among the groups.

  10. Serum leveis of inflammatory markers in type 2 diabetes patients with chronic periodontitis

    PubMed Central

    LONGO, Priscila Larcher; ARTESE, Hilana Paula Carillo; RABELO, Marianade Sousa; KAWAMOTO, Dione; FOZ, Adriana Moura; ROMITO, Giuseppe Alexandre; DIB, Sérgio Atala; MAYER, Marcia Pinto Alves

    2014-01-01

    Diabetes has been associated with periodontitis, but the mechanisms through which periodontal diseases affect the metabolic control remain unclear. Objective This study aimed to evaluate serum leveis of inflammatory markers, IL-8, IL-6 and monocyte chemoattractant protein 1 (MCP-1), in type 2 diabetic patients in the presence of chronic periodontitis. Material and Methods Forty two individuals were enrolled in this study and assigned to one of five groups: diabetes mellitus with inadequate glycemic control and periodontitis (DMI+P, n = 10), diabetes mellitus with adequate glycemic control and periodontitis (DMA+P, n = 10), diabetes mellitus without periodontitis (DM, n = 10), periodontitis without diabetes (P, n=6), and neither diabetes nor periodontitis (H, n = 6). Periodontal clinical examination included visible plaque index (PL), gingival bleeding index (GB), probing depth (PD), attachment level (AL) and bleeding on probing (BP). Glycemic control was evaluated by serum concentration of glycated hemoglobin (HbAlc). Inflammatory serum markers IL-8, IL-6 and (MCP-1) were measured by ELISA. Results DMI+P and DMA+P groups presented higher PD (p=0.025) and AL (p=0.003) values when compared to the P group. There were no significant differences among groups for IL-6, IL-8 and MCP-1 serum levels. Conclusions Although periodontitis was more severe in diabetic patients, the serum levels of the investigated inflammatory markers did not differ among the groups. PMID:24676580

  11. Omega-3 supplementation on inflammatory markers in patients with chronic Chagas cardiomyopathy: a randomized clinical study.

    PubMed

    Silva, Paula Simplício da; Mediano, Mauro Felippe Felix; Silva, Gilberto Marcelo Sperandio da; Brito, Patricia Dias de; Cardoso, Claudia Santos de Aguiar; Almeida, Cristiane Fonseca de; Sangenis, Luiz Henrique Conde; Pinheiro, Roberta Olmo; Hasslocher-Moreno, Alejandro Marcel; Brasil, Pedro Emmanuel Alvarenga Americano do; Sousa, Andrea Silvestre de

    2017-06-09

    Several studies have been focusing on the effect of omega-3 polyunsaturated fatty acids on modulation of inflammatory markers in several cardiopathies. Although immunoregulatory dysfunction has been associated to the chronic cardiac involvement in Chagas disease, there is no study examining the effects of omega-3 supplementation in these patients. We investigated the effects of omega-3 PUFAs on markers of inflammation and lipid profile in chronic Chagas cardiomyopathy patients. The present study was a single-center double-blind clinical trial including patients with chronic Chagas cardiomyopathy. Patients were randomly assigned to receive omega-3 PUFAs capsules (1.8g EPA and 1.2g DHA) or placebo (corn oil) during an 8-week period. Cytokines, fasting glucose, lipid, and anthropometric profiles were evaluated. Forty-two patients (23 women and 19 men) were included in the study and there were only two losses to follow-up during the 8-week period. Most of sociodemographic and clinical characteristics were similar between the groups at baseline, except for the cytokines IL-1β, IL-6, IL-8, IL-10, IL-17α, and IFNγ. The omega-3 PUFAs group demonstrated greater improvements in serum triglycerides (-21.1 vs. -4.1; p = 0.05) and IL-10 levels (-10.6 vs. -35.7; p = 0.01) in comparison to controls after 8 weeks of intervention. No further differences were observed between groups. Omega-3 PUFAs supplementation may favorably affect lipid and inflammatory profile in chronic Chagas cardiomyopathy patients, demonstrated by a decrease in triglycerides and improvements on IL-10 concentration. Further studies examining the clinical effects of omega-3 fatty acids supplementation in chronic Chagas cardiomyopathy are necessary. NCT01863576.

  12. Respiratory viruses, symptoms, and inflammatory markers in acute exacerbations and stable chronic obstructive pulmonary disease.

    PubMed

    Seemungal, T; Harper-Owen, R; Bhowmik, A; Moric, I; Sanderson, G; Message, S; Maccallum, P; Meade, T W; Jeffries, D J; Johnston, S L; Wedzicha, J A

    2001-11-01

    The effects of respiratory viral infection on the time course of chronic obstructive pulmonary disease (COPD) exacerbation were examined by monitoring changes in systemic inflammatory markers in stable COPD and at exacerbation. Eighty-three patients with COPD (mean [SD] age, 66.6 [7.1] yr, FEV(1), 1.06 [0.61] L) recorded daily peak expiratory flow rate and any increases in respiratory symptoms. Nasal samples and blood were taken for respiratory virus detection by culture, polymerase chain reaction, and serology, and plasma fibrinogen and serum interleukin-6 (IL-6) were determined at stable baseline and exacerbation. Sixty-four percent of exacerbations were associated with a cold occurring up to 18 d before exacerbation. Seventy-seven viruses (39 [58.2%] rhinoviruses) were detected in 66 (39.2%) of 168 COPD exacerbations in 53 (64%) patients. Viral exacerbations were associated with frequent exacerbators, colds with increased dyspnea, a higher total symptom count at presentation, a longer median symptom recovery period of 13 d, and a tendency toward higher plasma fibrinogen and serum IL-6 levels. Non-respiratory syncytial virus (RSV) respiratory viruses were detected in 11 (16%), and RSV in 16 (23.5%), of 68 stable COPD patients, with RSV detection associated with higher inflammatory marker levels. Respiratory virus infections are associated with more severe and frequent exacerbations, and may cause chronic infection in COPD. Prevention and early treatment of viral infections may lead to a decreased exacerbation frequency and morbidity associated with COPD.

  13. Comparison of tumor markers and inflammatory biomarkers in chronic obstructive pulmonary disease (COPD) exacerbations.

    PubMed

    Barouchos, Nikolaos; Papazafiropoulou, Athanasia; Iacovidou, Nicoletta; Vrachnis, Nikolaos; Barouchos, Nektarios; Armeniakou, Eleni; Dionyssopoulou, Vasiliki; Mathioudakis, Alexandros G; Christopoulou, Eleni; Koltsida, Spiridoula; Bassiakou, Eleni

    2015-04-01

    The aim of the present study was: (a) to measure levels of the tumor markers, Carcinoembryonic antigen (CEA), Cancer antigen 19-9 (CA19-9), Cancer antigen 125 (CA125), Neuron specific enolase (NSE) and Cytokeratin fragments 19 (CYFRA21-1); (b) to investigate any correlation between them and the inflammatory biomarkers C-reactive protein (CRP), Erythrocyte sedimentation rate (ESR) and white blood cells count (WBC), in patients with chronic obstructive pulmonary disease (COPD) exacerbation, who belong in groups of severity C and D, as classified by the Global Initiative for Chronic Obstructive Lung Disease (GOLD); (c) and finally, to compare these results in these two groups. Fifty-two patients with COPD exacerbation [35 male/17 female, mean age (± SD) 68.3 ± 6.4 years] were the study subjects, and were classified in severity groups C (n = 27) and D (n = 25), based on the spirometric classification, the number of exacerbations in the preceding year and the assessment of their symptoms by GOLD. Results. CEA and CA125 were increased in group D. In group C, there was a significant correlation between CRP and CA125 (p = 0.05). In group D, there was a significant correlation between WBC and NSE (p = 0.02), between CRP and CA19-9 (p = 0.02) and NSE (p < 0.001), and between the ESR and NSE (p = 0.03). CA125 (p = 0.01) and CA19-9 (p = 0.01) were significantly higher in group D compared to group C. In contrast, there was no significant difference in two groups for NSE, CEA and CYFRA21-1. Certain tumor markers were increased and were associated with increased levels of inflammatory biomarkers and with the disease severity. Inflammation might have a key pathogenetic role linking the above tumor markers with the severity of COPD.

  14. Protein-Bound Uremic Toxins from Gut Microbiota and Inflammatory Markers in Chronic Kidney Disease.

    PubMed

    Borges, Natália A; Barros, Amanda F; Nakao, Lia S; Dolenga, Carla J; Fouque, Denis; Mafra, Denise

    2016-11-01

    Protein-bound uremic toxins from gut microbiota tend to accumulate in chronic kidney disease (CKD) patients and are poorly removed by current dialysis techniques. These toxins induce inflammation and are associated with cardiovascular disease (CVD). The aim of this study was to report the relationship between uremic toxins and inflammatory and cardiovascular markers in CKD patients. This was a cross sectional study. Twenty-one nondialysis patients were included (43% men, 63.0 ± 7.8 years, glomerular filtration rate: 34.4 ± 12.5 mL/min) as well as 29 hemodialysis (HD) patients [58% men, 52.7 ± 10.3 years, time on dialysis 54 (31-94.5 months)]. Total levels of uremic toxins (IS, p-CS, and IAA) were assessed by high-performance liquid chromatography with fluorescence detection. C-reactive protein, Interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), and calprotectin plasma levels were determined by immunometric assays. HD patients presented higher inflammatory markers and uremic toxins levels than nondialysis patients. IL-6 levels were positively correlated with IS (r = 0.49; P = .03), p-CS (r = 0.35; P = .04) and IAA (r = 0.36; P = .03). A positive correlation was also observed between MCP-1 levels with IS (r = 0.72; P = .001), p-CS (r = 0.48; P = .001) and IAA (r = 0.75; P = .0001). Linear regression showed that IS was an independent predictor for IL-6 and MCP-1 levels after adjustment. Plasma uremic toxins were associated with higher IL-6 and MCP-1 levels in CKD patients, potentially playing a role in the development of CVD. Copyright © 2016 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.

  15. The Effect of Resistance Exercise on Inflammatory and Myogenic Markers in Patients with Chronic Kidney Disease

    PubMed Central

    Watson, Emma L.; Viana, Joao L.; Wimbury, David; Martin, Naomi; Greening, Neil J.; Barratt, Jonathan; Smith, Alice C.

    2017-01-01

    Background: Muscle wasting is a common complication of Chronic Kidney Disease (CKD) and is clinically important given its strong association with morbidity and mortality in many other chronic conditions. Exercise provides physiological benefits for CKD patients, however the molecular response to exercise remains to be fully determined. We investigated the inflammatory and molecular response to resistance exercise before and after training in these patients. Methods: This is a secondary analysis of a randomized trial that investigated the effect of 8 week progressive resistance training on muscle mass and strength compared to non-exercising controls. A sub-set of the cohort consented to vastus lateralis skeletal muscle biopsies (n = 10 exercise, n = 7 control) in which the inflammatory response (IL-6, IL-15, MCP-1 TNF-α), myogenic (MyoD, myogenin, myostatin), anabolic (P-Akt, P-eEf2) and catabolic events (MuRF-1, MAFbx, 14 kDa, ubiquitin conjugates) and overall levels of oxidative stress have been studied. Results: A large inflammatory response to unaccustomed exercise was seen with IL-6, MCP-1, and TNF-α all significantly elevated from baseline by 53-fold (P < 0.001), 25-fold (P < 0.001), and 4-fold (P < 0.001), respectively. This response was reduced following training with IL-6, MCP-1, and TNF-α elevated non-significantly by 2-fold (P = 0.46), 2.4-fold (P = 0.19), and 2.5-fold (P = 0.06), respectively. In the untrained condition, an acute bout of resistance exercise did not result in increased phosphorylation of Akt (P = 0.84), but this was restored following training (P = 0.01). Neither unaccustomed nor accustomed exercise resulted in a change in myogenin or MyoD mRNA expression (P = 0.88, P = 0.90, respectively). There was no evidence that resistance exercise training created a prolonged oxidative stress response within the muscle, or increased catabolism. Conclusions: Unaccustomed exercise creates a large inflammatory response within the muscle, which is no

  16. The beneficial role of anti-inflammatory dietary ingredients in attenuating markers of chronic low-grade inflammation in aging.

    PubMed

    Panickar, Kiran S; Jewell, Dennis E

    2015-08-01

    Aging in humans is associated with chronic low-grade inflammation (systemic), and this condition is sometimes referred to as "inflammaging". In general, canines also age similarly to humans, and such aging is associated with a decline in mobility, joint problems, weakened muscles and bones, reduced lean body mass, cancer, increased dermatological problems, decline in cognitive ability, reduced energy, decreased immune function, decreased renal function, and urinary incontinence. Each of these conditions is also associated with an increase in pro-inflammatory cytokines. An inflammatory state characterized by an increase in pro-inflammatory markers including but not restricted to tumor necrosis factor-α, interleukin-6, IL-1β, and C-reactive protein (CRP) is believed to contribute to or worsen a general decline in biological mechanisms responsible for physical function with aging. Nutritional management of inflammation in aging dogs is important in maintaining health. In particular, natural botanicals have bioactive components that appear to have robust anti-inflammatory effects and, when included in the diet, may contribute to a reduction in inflammation. While there are scientific data to support the anti-inflammatory effects and the efficacy of such bioactive molecules from botanicals, the clinical data are limited and more studies are needed to validate the efficacy of these ingredients. This review will summarize the role of dietary ingredients in reducing inflammatory molecules as well as review the evidence available to support the role of diet and nutrition in reducing chronic low-grade systemic inflammation in animal and human studies with a special reference to canines, where possible.

  17. Sweet bing cherries lower circulating concentrations of markers for chronic inflammatory diseases in healthy humans.

    PubMed

    Kelley, Darshan S; Adkins, Yuriko; Reddy, Aurosis; Woodhouse, Leslie R; Mackey, Bruce E; Erickson, Kent L

    2013-03-01

    A limited number of studies have demonstrated that some modulators of inflammation can be altered by the consumption of sweet cherries. We have taken a proteomics approach to determine the effects of dietary cherries on targeted gene expression. The purpose was then to determine changes caused by cherry consumption in the plasma concentrations of multiple biomarkers for several chronic inflammatory diseases in healthy humans with modestly elevated C-reactive protein (CRP; range, 1-14 mg/L; mean, 3.5 mg/L; normal, <1.0 mg/L). Eighteen men and women (45-61 y) supplemented their diets with Bing sweet cherries (280 g/d) for 28 d. Fasting blood samples were taken before the start of consuming the cherries (study d 7), 28 d after the initiation of cherry supplementation (d 35), and 28 d after the discontinuation (d 63). Of the 89 biomarkers assessed, cherry consumption for 28 d altered concentrations of 9, did not change those of 67, and the other 13 were below the detection limits. Cherry consumption decreased (P < 0.05) plasma concentrations of extracellular newly identified ligand for the receptor for advanced glycation end products (29.0%), CRP (20.1%), ferritin (20.3%), plasminogen activator inhibitor-1 (19.9%), endothelin-1 (13.7%), epidermal growth factor (13.2%), and IL-18 (8.1%) and increased that of IL-1 receptor antagonist (27.9%) compared with corresponding values on study d 7. The ferritin concentration continued to decrease between d 35 and 63 and it was significantly lower on d 63 than on d 7. Because the participants in this study were healthy, no clinical pathology end points were measured. However, results from the present study demonstrate that cherry consumption selectively reduced several biomarkers associated with inflammatory diseases.

  18. Peripheral Inflammatory Markers and Antioxidant Response during the Post-Acute and Chronic Phase after Severe Traumatic Brain Injury

    PubMed Central

    Licastro, Federico; Hrelia, Silvana; Porcellini, Elisa; Malaguti, Marco; Di Stefano, Cristina; Angeloni, Cristina; Carbone, Ilaria; Simoncini, Laura; Piperno, Roberto

    2016-01-01

    Traumatic brain injury (TBI) is a mechanical insult to the brain caused by external forces and associated with inflammation and oxidative stress. The patients may show different profiles of neurological recovery and a combination of oxidative damage and inflammatory processes can affect their courses. It is known that an overexpression of cytokines can be seen in peripheral blood in the early hours/days after the injury, but little is known about the weeks and months encompassing the post-acute and chronic phases. In addition, no information is available about the antioxidant responses mediated by the major enzymes that regulate reactive oxygen species levels: superoxide dismutase, catalase, peroxidases, and GSH-related enzymes. This study investigates the 6-month trends of inflammatory markers and antioxidant responses in 22 severe TBI patients with prolonged disorders of consciousness, consecutively recruited in a dedicated neurorehabilitation facility. Patients with a high degree of neurological impairment often show an uncertain outcome. In addition, the profiles of plasma activities were related to the neurological recovery after 12 months. Venous peripheral blood samples were taken blindly as soon as clinical signs and laboratory markers confirmed the absence of infections, 3 and 6 months later. The clinical and neuropsychological assessment continued up to 12 months. Nineteen patients completed the follow-up. In the chronic phase, persistent high plasma levels of cytokines can interfere with cognitive functioning and higher post-acute levels of cytokines [interferon (IFN)-γ, tumor necrosis factor (TNF)-α, IL1b, IL6] are associated with poorer cognitive recoveries 12 months later. Moreover, higher IFN-γ, higher TNF-α, and lower glutathione peroxidase activity are associated with greater disability. The results add evidence of persistent inflammatory response, provide information about long-term imbalance of antioxidant activity, and suggest that

  19. Peripheral Inflammatory Markers and Antioxidant Response during the Post-Acute and Chronic Phase after Severe Traumatic Brain Injury.

    PubMed

    Licastro, Federico; Hrelia, Silvana; Porcellini, Elisa; Malaguti, Marco; Di Stefano, Cristina; Angeloni, Cristina; Carbone, Ilaria; Simoncini, Laura; Piperno, Roberto

    2016-01-01

    Traumatic brain injury (TBI) is a mechanical insult to the brain caused by external forces and associated with inflammation and oxidative stress. The patients may show different profiles of neurological recovery and a combination of oxidative damage and inflammatory processes can affect their courses. It is known that an overexpression of cytokines can be seen in peripheral blood in the early hours/days after the injury, but little is known about the weeks and months encompassing the post-acute and chronic phases. In addition, no information is available about the antioxidant responses mediated by the major enzymes that regulate reactive oxygen species levels: superoxide dismutase, catalase, peroxidases, and GSH-related enzymes. This study investigates the 6-month trends of inflammatory markers and antioxidant responses in 22 severe TBI patients with prolonged disorders of consciousness, consecutively recruited in a dedicated neurorehabilitation facility. Patients with a high degree of neurological impairment often show an uncertain outcome. In addition, the profiles of plasma activities were related to the neurological recovery after 12 months. Venous peripheral blood samples were taken blindly as soon as clinical signs and laboratory markers confirmed the absence of infections, 3 and 6 months later. The clinical and neuropsychological assessment continued up to 12 months. Nineteen patients completed the follow-up. In the chronic phase, persistent high plasma levels of cytokines can interfere with cognitive functioning and higher post-acute levels of cytokines [interferon (IFN)-γ, tumor necrosis factor (TNF)-α, IL1b, IL6] are associated with poorer cognitive recoveries 12 months later. Moreover, higher IFN-γ, higher TNF-α, and lower glutathione peroxidase activity are associated with greater disability. The results add evidence of persistent inflammatory response, provide information about long-term imbalance of antioxidant activity, and suggest that

  20. Apo(a)-isoform size, nutritional status and inflammatory markers in chronic renal failure.

    PubMed

    Stenvinkel, P; Heimbürger, O; Tuck, C H; Berglund, L

    1998-05-01

    Atherosclerotic cardiovascular disease and malnutrition are widely recognized as leading causes of the increased morbidity and mortality observed in uremic patients. Levels of lipoprotein (a) [Lp(a)], an established cardiovascular risk factor, are elevated in uremic patients. Moreover, low serum albumin levels indicating malnutrition have been associated with elevated plasma Lp(a) levels in dialysis patients. However, serum albumin levels are also influenced by an inflammatory reaction. The present study was undertaken to further investigate the relationship between Lp(a), inflammation and malnutrition in patients with chronic renal failure (CRF) prior to the initiation of renal replacement therapy, and to investigate the potential relation between these factors and apo(a)-isoform size, an important determinant of plasma Lp(a) levels. A total of 83 patients (mean age 52 +/- 1 year) with terminal (creatinine clearance 9 +/- 1 ml/min) CRF were cross sectionally investigated. In addition to lipid parameters and apo(a)-isoform size, C-reactive protein (CRP), nutritional parameters including serum levels of albumin and body composition (dual energy x-ray absorptiometry), as well as a subjective global assessment (SGA) and the prevalence of cardiovascular disease (CVD) were evaluated. Malnourished patients (N = 39) had a significantly (P < 0.05) higher median plasma Lp(a) level (19.5 mg/dl) as compared to 44 well-nourished patients, (11.7 mg/dl). No difference was found for other lipid or lipoprotein parameters. A significant relationship was found between CRP and plasma Lp(a), whereas no significant relation was observed between plasma Lp(a) and serum albumin levels. The apo(a)-isoform distribution was similar among malnourished and well-nourished patients. There was no difference in nutritional parameters when comparing patients with small- and large-size apo(a) isoforms. However, a subgroup of patients (12%) with no detectable apo(a)-bands and low Lp(a) levels had

  1. Chronic oral infection with major periodontal bacteria Tannerella forsythia modulates systemic atherosclerosis risk factors and inflammatory markers

    PubMed Central

    Chukkapalli, Sasanka S.; Rivera-Kweh, Mercedes F.; Velsko, Irina M.; Chen, Hao; Zheng, Donghang; Bhattacharyya, Indraneel; Gangula, Pandu R.; Lucas, Alexandra R.; Kesavalu, Lakshmyya

    2015-01-01

    Tannerella forsythia is a Gram-negative anaerobic organism that inhabits the subgingival cavity and initiates connective tissue destruction and alveolar bone resorption in periodontal disease (PD). PD is a chronic immunoinflammatory disease and has been linked to several systemic diseases including atherosclerosis. This study evaluated the effects of a chronic oral infection with T. forsythia ATCC 43037 on the induction of PD, inflammatory markers and atherosclerosis risk factors in hyperlipidemic ApoEnull mice. Mice were orally infected for 12 and 24 weeks prior to euthanasia. Bacterial colonization of the oral cavity and bacteremia was confirmed via isolation of genomic DNA from oral plaque and tissues. Oral infection elicited significantly elevated levels of serum IgG and IgM antibodies and alveolar bone resorption compared to control mice. Tannerella forsythia-infected mice had increased serum amyloid A, and significantly reduced serum nitric oxide when compared to controls. Tannerella forsythia chronic infection also significantly increased serum lipoproteins suggesting altered cholesterol metabolism and potential for aortic inflammation. Despite enhanced acute phase reactants and altered lipid profiles, T. forsythia infection was associated with decreased aortic plaque. This study investigates the potential of a known periodontal bacterial pathogen found in atherosclerotic plaque in humans to accelerate atherosclerosis in hyperlipdemic mice. PMID:25663343

  2. Chronic oral infection with major periodontal bacteria Tannerella forsythia modulates systemic atherosclerosis risk factors and inflammatory markers.

    PubMed

    Chukkapalli, Sasanka S; Rivera-Kweh, Mercedes F; Velsko, Irina M; Chen, Hao; Zheng, Donghang; Bhattacharyya, Indraneel; Gangula, Pandu R; Lucas, Alexandra R; Kesavalu, Lakshmyya

    2015-04-01

    Tannerella forsythia is a Gram-negative anaerobic organism that inhabits the subgingival cavity and initiates connective tissue destruction and alveolar bone resorption in periodontal disease (PD). PD is a chronic immunoinflammatory disease and has been linked to several systemic diseases including atherosclerosis. This study evaluated the effects of a chronic oral infection with T. forsythia ATCC 43037 on the induction of PD, inflammatory markers and atherosclerosis risk factors in hyperlipidemic ApoE(null) mice. Mice were orally infected for 12 and 24 weeks prior to euthanasia. Bacterial colonization of the oral cavity and bacteremia was confirmed via isolation of genomic DNA from oral plaque and tissues. Oral infection elicited significantly elevated levels of serum IgG and IgM antibodies and alveolar bone resorption compared to control mice. Tannerella forsythia-infected mice had increased serum amyloid A, and significantly reduced serum nitric oxide when compared to controls. Tannerella forsythia chronic infection also significantly increased serum lipoproteins suggesting altered cholesterol metabolism and potential for aortic inflammation. Despite enhanced acute phase reactants and altered lipid profiles, T. forsythia infection was associated with decreased aortic plaque. This study investigates the potential of a known periodontal bacterial pathogen found in atherosclerotic plaque in humans to accelerate atherosclerosis in hyperlipdemic mice.

  3. Biologic markers of chronic GVHD.

    PubMed

    Pidala, J; Sarwal, M; Roedder, S; Lee, S J

    2014-03-01

    Biologic markers of chronic GVHD may provide insight into the pathogenesis of the syndrome, identify molecular targets for novel interventions, and facilitate advances in clinical management. Despite extensive work performed to date largely focused on prediction and diagnosis of the syndrome, little synthesis of findings and validation of promising candidate markers in independent populations has been performed. Studies suggest that risk for subsequent chronic GVHD development may be associated with donor-recipient genetic polymorphism, deficiency in regulatory immune cell populations (NK, Treg, DC2), and variation in inflammatory and immunoregulatory mediators post-HCT (increased TNFα, IL-10 and BAFF, and decreased TGFβ and IL-15). Established chronic GVHD is associated with alteration in immune cell populations (increased CD3(+) T cells, Th17, CD4(+) and CD8(+) effector memory cells, monocytes, CD86 expression, BAFF/B cell ratio, and deficiency of Treg, NK cells, and naïve CD8(+) T cells). Inflammatory and immunomodulatory factors (TNFα, IL-6, IL-1β, IL-8, sIL-2R, and IL-1Ra, BAFF, anti-dsDNA, sIL-2Rα, and sCD13) are also perturbed. Little is known about biologic markers of chronic GVHD phenotype and severity, response to therapy, and prognosis.

  4. Chronic Inflammatory Demyelinating Polyneuropathy

    PubMed Central

    Dimachkie, Mazen M.; Barohn, Richard J.

    2014-01-01

    Opinion statement Chronic Inflammatory polyneuropathies are an important group of neuromuscular disorders that present chronically and progress over more than 8 weeks, being referred to as chronic inflammatory demyelinating polyneuropathy (CIDP). Despite tremendous progress in elucidating disease pathogenesis, the exact triggering event remains unknown. Our knowledge regarding diagnosis and management of CIDP and its variants continues to expand, resulting in improved opportunities for identification and treatment. Most clinical neurologists will be involved in the management of patients with these disorders, and should be familiar with available therapies for CIDP. We review the distinctive clinical, laboratory, and electro-diagnostic features that aid in diagnosis. We emphasize the importance of clinical patterns that define treatment responsiveness and the most appropriate therapies in order to improve prognosis. PMID:23564314

  5. Effect of treatment of chronic periodontitis on levels of serum markers of acute-phase inflammatory and vascular responses.

    PubMed

    Ide, M; McPartlin, D; Coward, P Y; Crook, M; Lumb, P; Wilson, R F

    2003-04-01

    Recent epidemiological work suggests an association between periodontal disease severity and cardiovascular disease risk. This study aimed to ascertain if circulating levels of cardiovascular and systemic inflammatory markers could be modified following treatment of periodontal disease. Adult subjects were recruited from those awaiting periodontal treatment and randomised to either immediate (test, n=24) or delayed treatment (control, n=15). Demographic and clinical data were collected and venous blood was taken before and either 6 weeks after completion of treatment or after an equivalent 3-month control period. Periodontal examination included probing depth, loss of attachment, plaque scores and bleeding scores. Blood was analysed to determine serum and plasma fibrinogen, C-reactive protein, sialic acid, tumour necrosis factor-alpha and interleukin -6 and -1beta. Effects of treatment were assessed by paired tests and analysis of variance by treatment group with baseline covariates. Treatment improved plaque and bleeding scores and reduced probing depths (p<0.002). However, there were no statistically significant changes in levels of any of the systemic markers. Improvement in periodontal health did not influence the levels of vascular markers.

  6. The chronic effects of whey proteins on blood pressure, vascular function, and inflammatory markers in overweight individuals.

    PubMed

    Pal, Sebely; Ellis, Vanessa

    2010-07-01

    Limited evidence suggests that dairy whey protein may be the major dairy component that is responsible for health benefits currently associated with increased dairy consumption. Whey proteins may reduce blood pressure and improve cardiovascular health. This study evaluated the effects of whey protein supplementation on blood pressure, vascular function and inflammatory markers compared to casein and glucose (control) supplementation in overweight/obese individuals. The subjects were randomized to either whey protein, casein or glucose supplementation for 12 weeks according to a parallel design. In all, 70 men and women with a mean (+/-s.e.m.) BMI (kg/m(2)) of 31.3 +/- 0.8 completed the study. Systolic blood pressure (SBP) decreased significantly at week 6 compared to baseline in the whey and casein groups, (P = 0.028 and P = 0.020, respectively) and at week 12 (P = 0.020, and P = 0.017, respectively). Diastolic blood pressure (DBP) decreased significantly compared to baseline in the whey and casein groups (P = 0.038 and P = 0.042, respectively) at week 12. DBP decreased significantly in the whey and casein groups (P = 0.025, P = 0.038, respectively) at week 12 compared to the control group. Augmentation index (AI) was significantly lower from baseline at 12 weeks (P = 0.021) in the whey group. AI decreased significantly in the whey group at 12 weeks compared to control (P = 0.006) and casein (P = 0.006). There were no significant changes in inflammatory markers within or between groups. This study demonstrated that supplementation with whey protein improves blood pressure and vascular function in overweight and obese individuals.

  7. Chronic inflammatory demyelinating polyneuropathy.

    PubMed

    Gorson, Kenneth C; Katz, Jonathan

    2013-05-01

    Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is an immune disorder of the peripheral nervous system. This article highlights our current understanding of the condition along with its phenotypic variants that are encountered in clinical practice. The diagnostic evaluation of CIDP includes laboratory studies to detect associated medical conditions and electrodiagnostic studies to assess for demyelination. Current treatment options include corticosteroids, plasma exchange, and intravenous immune globulin, along with alternative therapies that may be used as corticosteroid-sparing agents or for treatment-refractory cases. Approximately 85% to 90% of patients eventually improve or stabilize with treatment, and the long-term prognosis of CIDP is favorable.

  8. High sensitive C-reactive protein as a systemic inflammatory marker and LDH-3 isoenzyme in chronic obstructive pulmonary disease.

    PubMed

    Nillawar, Anup N; Bardapurkar, J S; Bardapurkar, S J

    2012-01-01

    Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory disease, mainly due to tobacco smoke. Pulmonary function tests (PFTs) are mandatory to diagnose COPD which shows irreversible airway obstruction. This study was aimed at understanding the behavior of biochemical parameters such as high sensitive C-reactive protein (hs-CRP) and lactate dehydrogenase (LDH) isoenzymes in COPD. Cytoplasmic cellular enzymes, such as LDH in the extracellular space, although of no further metabolic function in this space, are of benefit because they serve as indicators suggestive of disturbances of the cellular integrity induced by pathological conditions. The lung pattern is characterized by proportional increases in isoenzymes 3, 4, and 5. Hs-CRP indicates low grade of systemic inflammation. Total (n = 45) patients of COPD (diagnosed on PFTs) were included. We followed the guidelines laid by the institute ethical committee. Investigations performed on the serum were the serum for hs-CRP, LDH isoenzymes on agarose gel electrophoresis. The results obtained showed that the value of hs-CRP was 4.6 ± 0.42 mg/L. The isoenzymes pattern was characterized by an increase in LDH-3 and LDH-4 fractions. This is evident even in those patients with normal LDH (n = 13) levels. This study states that there is a moderate positive correlation in between CRP and LDH-3 (r = 0.33; P = 0.01). Raised LDH-3 levels do not correlate with FEV(1) % (forced expiratory volume in first second) predicted. Moreover, it associates positively with hs-CRP and smoking status and negatively with body mass index. This underlines the potential of these parameters to complement the present system of staging which is solely based upon FEV(1) % predicted.

  9. Chronic inflammatory systemic diseases

    PubMed Central

    Straub, Rainer H.; Schradin, Carsten

    2016-01-01

    It has been recognized that during chronic inflammatory systemic diseases (CIDs) maladaptations of the immune, nervous, endocrine and reproductive system occur. Maladaptation leads to disease sequelae in CIDs. The ultimate reason of disease sequelae in CIDs remained unclear because clinicians do not consider bodily energy trade-offs and evolutionary medicine. We review the evolution of physiological supersystems, fitness consequences of genes involved in CIDs during different life-history stages, environmental factors of CIDs, energy trade-offs during inflammatory episodes and the non-specificity of CIDs. Incorporating bodily energy regulation into evolutionary medicine builds a framework to better understand pathophysiology of CIDs by considering that genes and networks used are positively selected if they serve acute, highly energy-consuming inflammation. It is predicted that genes that protect energy stores are positively selected (as immune memory). This could explain why energy-demanding inflammatory episodes like infectious diseases must be terminated within 3–8 weeks to be adaptive, and otherwise become maladaptive. Considering energy regulation as an evolved adaptive trait explains why many known sequelae of different CIDs must be uniform. These are, e.g. sickness behavior/fatigue/depressive symptoms, sleep disturbance, anorexia, malnutrition, muscle wasting—cachexia, cachectic obesity, insulin resistance with hyperinsulinemia, dyslipidemia, alterations of steroid hormone axes, disturbances of the hypothalamic-pituitary-gonadal (HPG) axis, hypertension, bone loss and hypercoagulability. Considering evolved energy trade-offs helps us to understand how an energy imbalance can lead to the disease sequelae of CIDs. In the future, clinicians must translate this knowledge into early diagnosis and symptomatic treatment in CIDs. PMID:26817483

  10. Chronic inflammatory demyelinating polyneuropathy.

    PubMed

    Vanasse, Michel; Rossignol, Elsa; Hadad, Elie

    2013-01-01

    Chronic inflammatory demyelinating polyneuropathy (CIDP) is characterized clinically by a progressive symmetrical weakness evolving over a period of at least 2 months. There is increased CSF protein and conduction block, reduced nerve conduction velocities, increased distal latencies, and/or absent F wave or prolonged F wave latency in two or more nerves. Incidence is lower in children (10 times less) than in adults, and the condition presents in an acute or subacute manner with frequent relapses. It is not associated with other systemic diseases such as neoplasia, diabetes mellitus, or monoclonal gammopathies. It appears to be immune-related as a variety of humoral and cellular autoimmune mechanisms have been implicated. Treatment is based on results obtained in randomized clinical trials (RCTs) conducted in adults as such studies are lacking in the pediatric population. The evolution of CIDP is more favorable in children than in adults, with 80-100% response rates to standard treatments (steroids, intravenous immunoglobulins, and/or plasmapheresis) and excellent outcome with complete functional recovery in most patients. Cases refractory to standard therapies do exist in children, for which azathioprine, methotrexate, and mycophenolate mofetil alone or more often in association with other treatments have been used. However, safety and efficacy data are still insufficient to give specific recommendations regarding the optimal choice.

  11. Chronic inflammatory demyelinating polyneuropathy.

    PubMed

    Lewis, Richard A

    2017-10-01

    As a syndrome with typical and atypical cases, chronic inflammatory demyelinating polyneuropathy (CIDP) has been a difficult disorder to diagnose and treat. The pathophysiologic basis for CIDP has not been established, contributing to the challenges in dealing with these patients. However, as one of only a handful of treatable peripheral neuropathies, there has been a tendency to diagnose CIDP to attempt a therapeutic intervention. We are also aware that there has also been overtreatment of some patients. This combination of overdiagnosis and prolonged treatment has been a concern. This chapter will review these challenges and discuss recent findings that will lead to improved diagnosis and treatment. The factors leading to misdiagnosis of CIDP were explored in a cohort of patients referred to a neuromuscular center. On a more positive note, the identification of two disorders with antibodies directed at paranodal constituents has excited the field. Treatment options have increased and been clarified. Pulse corticosteroids have been compared with oral prednisone and with intravenous immunoglobulin. The clinical trial of subcutaneous immunoglobulin in CIDP has shown both efficacy and a very low side effect profile adding to our therapeutic options. The current review will identify recent developments that show both the challenges and the exciting growth in our ability to diagnose and treat CIDP.

  12. Chronic inflammatory demyelinating polyneuropathy.

    PubMed

    Mathey, Emily K; Pollard, John D

    2013-10-15

    Chronic inflammatory demyelinating polyneuropathy (CIDP) is the commonest treatable neuropathy in the western world. Untreated it may result in severe disability but if diagnosed and treated early there is effective treatment for the majority of patients. Typical CIDP is readily recognised but the diagnosis of other subgroups can be more challenging. The pathology of polyradiculoneuropathies such as CIDP characteristically affects the most proximal regions of the peripheral nervous system, nerve roots and major plexuses. It is important to test these regions with electrodiagnostic studies since routine neurophysiology may not encounter regions of pathology. Although accepted as an autoimmune disorder with an underlying immunopathology involving T cell and B cell responses, there is no agreement on major target antigens; however recent studies have highlighted a role for molecules in non compact myelin which play an essential role in the formation and maintenance of the nodal structures and hence in the function of ion channels central to saltatory conduction. Controlled trials have proven the efficacy of corticosteroid, intravenous immunoglobulin and plasma exchange in the short term and intravenous immunoglobulin also in the long term. Immunosuppressive agents are widely used but their efficacy has not been proven in controlled trials. Recent trials have shown the importance of attempting treatment withdrawal in patients apparently in remission to conserve treatments that are very expensive and in short supply, since a significant proportion of patients may enter long lasting remission following short term therapy. For the relatively small group of patients who do not respond to these first line therapies new agents including monoclonal antibodies may have a role.

  13. Systemic Inflammatory Marker CRP Was Better Predictor of Readmission for AECOPD Than Sputum Inflammatory Markers.

    PubMed

    Jing, Zhang; Chun, Chang; Ning, Shen; Hong, Zhu; Bei, He; Wan-Zhen, Yao

    2016-03-01

    Acute exacerbation of chronic obstructive pulmonary disease (AECOPD) readmission contributes considerably to the worse outcomes for COPD patients. Predictors for readmission include some socio-demographic variables and the severity of the underlying disease, however, few evidence suggested whether persistently heightened airway or systemic inflammation was related to recurrence of AECOPD. The aim of this study was to evaluate role of airway and systemic inflammatory biomarkers during AECOPD on predicting readmission for AECOPD. Consecutive hospitalized patients with AECOPD were recruited. Inflammatory and clinical indices were evaluated at the day of admission before starting therapy and the day of planned discharge (day 10-14). Predictors for readmission were assessed by binary logistic regression model. 93 patients were included with 51 patients (54.8%) were readmitted due to AECOPD at least once during 1 year following the index admission. The logistic regression model indicated that age (OR=1.072, 95%CI: 1.012-1.135, P=.017), hs-CRP (high sensitive-C reactive protein) at day 14 (OR=1.392, 95%CI: 1.131-1.712, P=.002), CAT value at day 14 (OR=1.12, 95%CI: 1.031-1.217, P=.007) were the independent variables statistically significant in predicting rehospitalization. Systemic inflammatory marker CRP was a better predictor of readmission than sputum inflammatory markers. CAT score and age were also useful to predict readmission. Copyright © 2014 SEPAR. Published by Elsevier Espana. All rights reserved.

  14. Statin Effects on Exacerbation Rates, Mortality, and Inflammatory Markers in Patients with Chronic Obstructive Pulmonary Disease: A Review of Prospective Studies.

    PubMed

    Howard, Meredith L; Vincent, Ashley H

    2016-05-01

    Chronic obstructive pulmonary disease (COPD) is a debilitating, irreversible disease with currently available therapies targeting symptom control and exacerbation reduction. A need for alternative disease-modifying therapies remains, specifically those that may have antiinflammatory and immunomodulatory properties that impact the pathophysiologic components of COPD. Statin drugs, the current gold standard for the treatment of dyslipidemia and prevention of cardiovascular disease (CVD), contain properties that affect the inflammatory disease processes seen in COPD. Several retrospective studies have demonstrated that statins may have a benefit in the reduction of morbidity and mortality in patients with COPD. This has led to prospective trials evaluating the impact of statins on various COPD-related outcomes. This article reviews the current body of prospective evidence for use of statins in patients with COPD. A search of the PubMed/Medline database of English-language articles was conducted from 1964 through November 2015; references of relevant articles were also reviewed for qualifying studies. Prospective studies of all types relating to statin use in patients with COPD were included if they had COPD- or respiratory-related outcomes; ultimately, eight studies were identified for this review. Statin effects on exacerbation rates, mortality, and inflammatory markers in patients with COPD are discussed. Strong prospective evidence does not currently exist to suggest that statins provide a clinical benefit in patients with COPD who do not have other CVD risk factors. Benefits from statins that have been illustrated are likely explained by their impact on underlying CVD risk factors rather than the COPD disease process. An opportunity exists for unanswered questions to be addressed in future studies. © 2016 Pharmacotherapy Publications, Inc.

  15. A comparison of patients with Q fever fatigue syndrome and patients with chronic fatigue syndrome with a focus on inflammatory markers and possible fatigue perpetuating cognitions and behaviour.

    PubMed

    Keijmel, Stephan P; Saxe, Johanna; van der Meer, Jos W M; Nikolaus, Stephanie; Netea, Mihai G; Bleijenberg, Gijs; Bleeker-Rovers, Chantal P; Knoop, Hans

    2015-10-01

    Comparison of Q fever fatigue syndrome (QFS) and chronic fatigue syndrome (CFS) patients, with a focus on markers of inflammation and fatigue-related cognitive-behavioural variables. Data from two independent prospective studies on QFS (n=117) and CFS (n=173), respectively, were pooled and analyzed. QFS patients were less often female, had a higher BMI, and had less often received treatment for depression before the onset of symptoms. After controlling for symptom duration and correcting for differences in diagnostic criteria for QFS and CFS with respect to the level of impairment and the presence of additional symptoms, differences in the proportion of females and BMI remained significant. After correction, QFS patients were also significantly older. In all analyses QFS patients were as fatigued and distressed as CFS patients, but reported less additional symptoms. QFS patients had stronger somatic attributions, and higher levels of physical activity. No differences were found with regard to inflammatory markers and in other fatigue-related cognitive-behavioural variables. The relationship between cognitive-behavioural variables and fatigue, previously established in CFS, could not be confirmed in QFS patients with the exception of the negative relationship between physical activity and fatigue. Differences and similarities between QFS and CFS patients were found. Although the relationship between perpetuating factors and fatigue previously established in CFS could not be confirmed in QFS patients, the considerable overlap in fatigue-related cognitive-behavioural variables and the relationship found between physical activity and fatigue may suggest that behavioural interventions could reduce fatigue severity in QFS patients. Copyright © 2015 Elsevier Inc. All rights reserved.

  16. Protective Effect of Bioactivity Guided Fractions of Ziziphus jujuba Mill. Root Bark against Hepatic Injury and Chronic Inflammation via Inhibiting Inflammatory Markers and Oxidative Stress

    PubMed Central

    Kandimalla, Raghuram; Dash, Suvakanta; Kalita, Sanjeeb; Choudhury, Bhaswati; Malampati, Sandeep; Kalita, Kasturi; Kalita, Bhupalee; Devi, Rajlakshmi; Kotoky, Jibon

    2016-01-01

    The tribal communities of North Eastern India rely on herbal medicine to cure various disease conditions. Ziziphus jujuba Mill. (Rhamnaceae) is one of such medicinal plants used for curing liver ailments, insomnia, anemia, diarrhea, diabetic complications, cancer, and loss of appetite. The present study was aimed to describe the protective ability of Z. jujuba root bark (ZJRB) against hepatic injury and chronic inflammation. Bioactivity guided fractionation of Z. jujuba methanol extract (ZJME) was performed using different solvents of increasing polarity viz. hexane (ZJHF), chloroform (ZJCF), ethyl acetate (ZJEAF), water (ZJWF), and residue (ZJMR). In vitro antioxidant results revealed that both ZJME and ZJWF possess strong antioxidant activity among all the fractions and mother extract tested. Further, ZJME and ZJWF showed significant protection against CCl4 intoxicated HepG2 cell lines by means of increased cell viability and decreased LDH levels compared to control group. ZJME at 200, 400 mg/kg and ZJWF at 50, 100 mg/kg inhibited the lipid peroxidation and significantly restored the liver function markers (AST, ALT, ALP, LDH, SOD, and CAT) and cytokine levels (TNF-α, Il-1β, and Il-10) in CCl4 induced acute liver damage in rats. All the results were comparable with standard drug silymarin which was further confirmed by histopathology analysis of liver. Similarly, inflammation and increase inflammatory cytokines levels of carrageenan induced paw edema in rats have been refurbished to normal levels on par with the standard drug indomethacin. ZJWF demonstrated potent response than ZJME in all the biological tests conducted. The results of the study signify the ability of ZJRB as good therapeutic agent for liver toxicity and chronic inflammation. PMID:27656145

  17. Preventive rather than therapeutic treatment with high fiber diet attenuates clinical and inflammatory markers of acute and chronic DSS-induced colitis in mice.

    PubMed

    Silveira, Ana Letícia Malheiros; Ferreira, Adaliene Versiani Matos; de Oliveira, Marina Chaves; Rachid, Milene Alvarenga; da Cunha Sousa, Larissa Fonseca; Dos Santos Martins, Flaviano; Gomes-Santos, Ana Cristina; Vieira, Angelica Thomaz; Teixeira, Mauro Martins

    2017-02-01

    Inflammatory bowel diseases (IBDs) are chronic inflammatory disorders with important impact on global health. Prebiotic and probiotic strategies are thought to be useful in the context of experimental IBD. Here, we compared the effects of preventive versus therapeutic treatment with a high fiber diet (prebiotic) in combination or not with Bifidobacterium longum (probiotic) in a murine model of chronic colitis. Colitis was induced by adding dextran sulfate sodium (DSS) to drinking water for 6 days (acute colitis) or for 5 cycles of DSS (chronic colitis). Administration of the high fiber diet protected from acute colitis. Protection was optimal when diet was started 20 days prior to DSS. A 5-day pretreatment with acetate, a short-chain fatty acid, provided partial protection against acute colitis. In chronic colitis, pretreatment with the high fiber diet attenuated clinical and inflammatory parameters of disease. However, when the treatment with the high fiber diet started after disease had been established, overall protection was minimal. Similarly, delayed treatment with acetate or B. longum did not provide any protection even when the probiotic was associated with the high fiber diet. Preventive use of a high fiber diet or acetate clearly protects mice against acute and chronic damage induced by DSS in mice. However, protection is lost when therapies are initiated after disease has been established. These results suggest that any therapy aimed at modifying the gut environment (e.g., prebiotic or probiotic strategies) should be given early in the course of disease.

  18. Challenges in pediatric chronic inflammatory demyelinating polyneuropathy.

    PubMed

    Haliloğlu, Göknur; Yüksel, Deniz; Temoçin, Cağri Mesut; Topaloğlu, Haluk

    2016-12-01

    Chronic inflammatory demyelinating neuropathy, a treatable immune-mediated disease of the peripheral nervous system is less common in childhood compared to adults. Despite different sets of diagnostic criteria, lack of a reliable biologic marker leads to challenges in diagnosis, follow-up and treatment. Our first aim was to review clinical presentation, course, response to treatment, and prognosis in our childhood patients. We also aimed to document diagnostic and therapeutic pitfalls and challenges at the bedside. Our original cohort consisted of 23 pediatric patients who were referred to us with a clinical diagnosis of chronic inflammatory demyelinating neuropathy. Seven patients reaching to an alternative diagnosis were excluded. In the remaining patients, diagnostic, treatment and follow-up data were compared in typical patients who satisfied both clinical and electrodiagnostic criteria and atypical patients who failed to meet minimal research chronic inflammatory demyelinating neuropathy electrodiagnostic requirements. Eight of 16 patients (50%) met the minimal chronic inflammatory demyelinating neuropathy research diagnostic requirements. There was only a statistically significant difference (p = 0.010) in terms of European Neuromuscular Centre childhood chronic inflammatory diagnostic mandatory clinical criteria between the two groups. Misdiagnosis due to errors in electrophysiological interpretation (100%, n = 8), cerebrospinal fluid cytoalbuminologic dissociation (100%, n = 4 and/or subjective improvement on any immunotherapy modality (80 ± 19.27%)) was frequent. Pediatric CIDP is challenging in terms of diagnostic and therapeutic pitfalls at the bedside. Diagnostic errors due to electrophysiological interpretation, cerebrospinal fluid cytoalbuminologic dissociation, and/or subjective improvement on immunotherapy should be considered.

  19. Inflammatory Markers and Breast Cancer Risk

    DTIC Science & Technology

    2010-07-01

    1 AD_________________ AWARD NUMBER: W81XWH-06- 1 -0533 TITLE: Inflammatory markers and breast...collection of information is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources...collection of information if it does not display a currently valid OMB control number. PLEASE DO NOT RETURN YOUR FORM TO THE ABOVE ADDRESS. 1 . REPORT

  20. Inflammatory Markers and Breast Cancer Risk

    DTIC Science & Technology

    2011-07-01

    06- 1 -0533 TITLE: Inflammatory Markers and Breast Cancer Risk PRINCIPAL INVESTIGATOR: Dr. Brenda Diergaarde...0188 Public reporting burden for this collection of information is estimated to average 1 hour per response, including the time for reviewing...FORM TO THE ABOVE ADDRESS. 1 . REPORT DATE (DD-MM-YYYY) 2. REPORT TYPE 3. DATES COVERED (From - To) 4. TITLE AND SUBTITLE 5a. CONTRACT NUMBER

  1. Diagnosing anemia in inflammatory bowel disease: beyond the established markers.

    PubMed

    Oustamanolakis, Pantelis; Koutroubakis, Ioannis E; Kouroumalis, Elias A

    2011-10-01

    The main types of anemia in inflammatory bowel disease (IBD) are iron deficiency anemia (IDA) and anemia of inflammatory etiology, or anemia of chronic disease (ACD). In the management of IBD patients with anemia it is essential for the physician to diagnose the type of anemia in order to decide in an evidence-based manner for the appropriate treatment. However, the assessment of iron status in IBD in many cases is rather difficult due to coexistent inflammation. For this assessment several indices and markers have been suggested. Ferritin, seems to play a central role in the definition and diagnosis of anemia in IBD and transferrin, transferrin saturation (Tsat), and soluble transferrin receptors are also valuable markers. All these biochemical markers have several limitations because they are not consistently reliable indices, since they are influenced by factors other than changes in iron balance. In this review, in addition to them, we discuss the newer alternative markers for iron status that may be useful when serum ferritin and Tsat are not sufficient. The iron metabolism regulators, hepcidin and prohepcidin, are still under investigation in IBD. Erythrocytes parameters like the red cell distribution width (RDW) and the percentage of hypochromic red cells as well as reticulocyte parameters such as hemoglobin concentration of reticulocytes, red blood cell size factor and reticulocyte distribution width could be useful markers for the evaluation of anemia in IBD.

  2. [Inflammatory markers in schizophrenia in aged].

    PubMed

    Androsova, L V; Mikhaĭlova, N M; Zozulia, S A; Dupin, A M; Kliushnik, T P

    2014-01-01

    To identify inflammatory markers in schizophrenia in aged. The main group included 29 patients with schizophrenia, mean age 72.1 ± 6.9 years. A comparison group comprised 34 patients with Alzheimer's disease, mean age 73.4 ± 7.9 years. Seven plasma inflammatory indicators were determined. There was a significant increase in the activity/content of acute inflammation stage proteins: α1-proteinase inhibitor and C-reactive protein as well as anti-inflammatory interleukin-10 compared to the controls while the activity of other inflammatory molecules (leukocyte elastase, tumor necrosis factor alpha, interleukin-1 receptor antagonist) was not changed. No correlations between immunological parameters and clinical presentations were found. The results suggest that inflammation does not play a significant role in the remote stages of schizophrenia, in contrast to earlier stages of the disease, and the activity of the pathological process decreased in the late stages. These characteristics can reflect the body reactivity in elderly patients.

  3. Associations of Coffee Drinking with Systemic Immune and Inflammatory Markers.

    PubMed

    Loftfield, Erikka; Shiels, Meredith S; Graubard, Barry I; Katki, Hormuzd A; Chaturvedi, Anil K; Trabert, Britton; Pinto, Ligia A; Kemp, Troy J; Shebl, Fatma M; Mayne, Susan T; Wentzensen, Nicolas; Purdue, Mark P; Hildesheim, Allan; Sinha, Rashmi; Freedman, Neal D

    2015-07-01

    Coffee drinking has been inversely associated with mortality as well as cancers of the endometrium, colon, skin, prostate, and liver. Improved insulin sensitivity and reduced inflammation are among the hypothesized mechanisms by which coffee drinking may affect cancer risk; however, associations between coffee drinking and systemic levels of immune and inflammatory markers have not been well characterized. We used Luminex bead-based assays to measure serum levels of 77 immune and inflammatory markers in 1,728 older non-Hispanic Whites. Usual coffee intake was self-reported using a food frequency questionnaire. We used weighted multivariable logistic regression models to examine associations between coffee and dichotomized marker levels. We conducted statistical trend tests by modeling the median value of each coffee category and applied a 20% false discovery rate criterion to P values. Ten of the 77 markers were nominally associated (P trend < 0.05) with coffee drinking. Five markers withstood correction for multiple comparisons and included aspects of the host response namely chemotaxis of monocytes/macrophages (IFNγ, CX3CL1/fractalkine, CCL4/MIP-1β), proinflammatory cytokines (sTNFRII), and regulators of cell growth (FGF-2). Heavy coffee drinkers had lower circulating levels of IFNγ [odds ratios (OR), 0.35; 95% confidence intervals (CI), 0.16-0.75], CX3CL1/fractalkine (OR, 0.25; 95% CI, 0.10-0.64), CCL4/MIP-1β (OR, 0.48; 95% CI, 0.24-0.99), FGF-2 (OR, 0.62; 95% CI, 0.28-1.38), and sTNFRII (OR, 0.34; 95% CI, 0.15-0.79) than non-coffee drinkers. Lower circulating levels of inflammatory markers among coffee drinkers may partially mediate previously observed associations of coffee with cancer and other chronic diseases. Validation studies, ideally controlled feeding trials, are needed to confirm these associations. ©2015 American Association for Cancer Research.

  4. Hypertrophic osteoarthropathy of chronic inflammatory bowel disease

    SciTech Connect

    Oppenheimer, D.A.; Jones, H.H.

    1982-12-01

    The case of a 14-year old girl with painful periostitis and ulcerative colitis is reported. The association of chronic inflammatory bowel disease with osteoarthropathy is rare and has previously been reported in eight patients. The periosteal reaction found in association with inflammatory bowel disease is apparently related to a chronic disease course and may cause extreme localized pain.

  5. Inflammatory and oncogenic roles of a tumor stem cell marker doublecortin-like kinase (DCLK1) in virus-induced chronic liver diseases.

    PubMed

    Ali, Naushad; Chandrakesan, Parthasarathy; Nguyen, Charles B; Husain, Sanam; Gillaspy, Allison F; Huycke, Mark; Berry, William L; May, Randal; Qu, Dongfeng; Weygant, Nathaniel; Sureban, Sripathi M; Bronze, Michael S; Dhanasekaran, Danny N; Houchen, Courtney W

    2015-08-21

    Hepatocellular carcinoma (HCC) is the third most common cause of cancer-related mortality worldwide. We previously showed that a tumor/cancer stem cell (CSC) marker, doublecortin-like kinase (DCLK1) positively regulates hepatitis C virus (HCV) replication, and promotes tumor growth in colon and pancreas. Here, we employed transcriptome analysis, RNA interference, tumor xenografts, patient's liver tissues and hepatospheroids to investigate DCLK1-regulated inflammation and tumorigenesis in the liver. Our studies unveiled novel DCLK1-controlled feed-forward signaling cascades involving calprotectin subunit S100A9 and NFκB activation as a driver of inflammation. Validation of transcriptome data suggests that DCLK1 co-expression with HCV induces BRM/SMARCA2 of SW1/SNF1 chromatin remodeling complexes. Frequently observed lymphoid aggregates including hepatic epithelial and stromal cells of internodular septa extensively express DCLK1 and S100A9. The DCLK1 overexpression also correlates with increased levels of S100A9, c-Myc, and BRM levels in HCV/HBV-positive patients with cirrhosis and HCC. DCLK1 silencing inhibits S100A9 expression and hepatoma cell migration. Normal human hepatocytes (NHH)-derived spheroids exhibit CSC properties. These results provide new insights into the molecular mechanism of the hepatitis B/C-virus induced liver inflammation and tumorigenesis via DCLK1-controlled networks. Thus, DCLK1 appears to be a novel therapeutic target for the treatment of inflammatory diseases and HCC.

  6. Inflammatory and oncogenic roles of a tumor stem cell marker doublecortin-like kinase (DCLK1) in virus-induced chronic liver diseases

    PubMed Central

    Ali, Naushad; Chandrakesan, Parthasarathy; Nguyen, Charles B.; Husain, Sanam; Gillaspy, Allison F.; Huycke, Mark; Berry, William L.; May, Randal; Qu, Dongfeng; Weygant, Nathaniel; Sureban, Sripathi M.; Bronze, Michael S.; Dhanasekaran, Danny N.; Houchen, Courtney W.

    2015-01-01

    Hepatocellular carcinoma (HCC) is the third most common cause of cancer-related mortality worldwide. We previously showed that a tumor/cancer stem cell (CSC) marker, doublecortin-like kinase (DCLK1) positively regulates hepatitis C virus (HCV) replication, and promotes tumor growth in colon and pancreas. Here, we employed transcriptome analysis, RNA interference, tumor xenografts, patient's liver tissues and hepatospheroids to investigate DCLK1-regulated inflammation and tumorigenesis in the liver. Our studies unveiled novel DCLK1-controlled feed-forward signaling cascades involving calprotectin subunit S100A9 and NFκB activation as a driver of inflammation. Validation of transcriptome data suggests that DCLK1 co-expression with HCV induces BRM/SMARCA2 of SW1/SNF1 chromatin remodeling complexes. Frequently observed lymphoid aggregates including hepatic epithelial and stromal cells of internodular septa extensively express DCLK1 and S100A9. The DCLK1 overexpression also correlates with increased levels of S100A9, c-Myc, and BRM levels in HCV/HBV-positive patients with cirrhosis and HCC. DCLK1 silencing inhibits S100A9 expression and hepatoma cell migration. Normal human hepatocytes (NHH)-derived spheroids exhibit CSC properties. These results provide new insights into the molecular mechanism of the hepatitis B/C-virus induced liver inflammation and tumorigenesis via DCLK1-controlled networks. Thus, DCLK1 appears to be a novel therapeutic target for the treatment of inflammatory diseases and HCC. PMID:25948779

  7. Unfulfilled inflammatory resolution leads to chronic inflammatory diseases.

    PubMed

    Musk, Philip

    2004-06-01

    Extract: Inflammatory conditions, particularly those that involve chronic inflammation, represent an area of great interest to the pharmaceutical industry. Regulated as they are by a diverse array of ligand-receptor interactions, inflammatory responses are amenable to small molecule pharmaceutical intervention and a wide variety of anti-histamines and anti-inflammatory treatments. Both steroidal and non-steroidal treatments have been developed to treat pro-inflammatory conditions. In their review, Gilroy et al. (2004) present the case for developing novel anti-inflammatory drugs not by finding more effective inhibitors of the inflammatory response, but by developing small molecule drugs that positively regulate the processes and mechanisms by which inflammatory responses are attenuated (i.e., the little known process of inflammatory resolution).

  8. Associations of coffee drinking with systemic immune and inflammatory markers

    PubMed Central

    Loftfield, Erikka; Shiels, Meredith S.; Graubard, Barry I.; Katki, Hormuzd A.; Chaturvedi, Anil K.; Trabert, Britton; Pinto, Ligia A.; Kemp, Troy J.; Shebl, Fatma M.; Mayne, Susan T.; Wentzensen, Nicolas; Purdue, Mark P.; Hildesheim, Allan; Sinha, Rashmi; Freedman, Neal D.

    2015-01-01

    Background Coffee drinking has been inversely associated with mortality as well as cancers of the endometrium, colon, skin, prostate, and liver. Improved insulin sensitivity and reduced inflammation are among the hypothesized mechanisms by which coffee drinking may affect cancer risk; however, associations between coffee drinking and systemic levels of immune and inflammatory markers have not been well characterized. Methods We used Luminex bead-based assays to measure serum levels of 77 immune and inflammatory markers in 1,728 older non-Hispanic Whites. Usual coffee intake was self-reported using a food frequency questionnaire. We used weighted multivariable logistic regression models to examine associations between coffee and dichotomized marker levels. We conducted statistical trend tests by modeling the median value of each coffee category and applied a 20% false discovery rate criterion to P-values. Results Ten of the 77 markers were nominally associated (P-value for trend<0.05) with coffee drinking. Five markers withstood correction for multiple comparisons and included aspects of the host response namely chemotaxis of monocytes/macrophages (IFNγ, CX3CL1/fractalkine, CCL4/MIP-1β), pro-inflammatory cytokines (sTNFRII) and regulators of cell growth (FGF-2). Heavy coffee drinkers had lower circulating levels of IFNγ (OR=0.35; 95% CI 0.16–0.75), CX3CL1/fractalkine (OR=0.25; 95% CI 0.10–0.64), CCL4/MIP-1β (OR=0.48; 95% CI 0.24–0.99), FGF-2 (OR=0.62; 95% CI 0.28–1.38), and sTNFRII (OR=0.34; 95% CI 0.15–0.79) than non-coffee drinkers. Conclusions Lower circulating levels of inflammatory markers among coffee drinkers may partially mediate previously observed associations of coffee with cancer and other chronic diseases. Impact Validation studies, ideally controlled feeding trials, are needed to confirm these associations. PMID:25999212

  9. Diet and diet combined with chronic aerobic exercise decreases body fat mass and alters plasma and adipose tissue inflammatory markers in obese women.

    PubMed

    Lakhdar, Nadia; Denguezli, Myriam; Zaouali, Monia; Zbidi, Abdelkrim; Tabka, Zouhair; Bouassida, Anissa

    2013-12-01

    The purpose of this study was to investigate the effect of 6 months aerobic exercise and diet alone or in combination on markers of inflammation (MOI) in circulation and in adipose abdominal tissue (AT) in obese women. Thirty obese subjects were randomized into a 24-week intervention: (1) exercise (EX), (2) diet (DI), and (3) exercise and diet (EXD). Blood samples were collected at baseline, after 12 and 24 weeks. AT biopsies were obtained only at baseline and after 24 weeks. In the EXD and DI groups, the fat loss was after 12 weeks was -13.74 and -7.8 % (P < 0.01) and after 24 weeks was -21.82 and -17 % (P < 0.01) with no changes in the EX group. After 12 and 24 weeks, maximal oxygen consumption (VO2max) was increased by 21.81-39.54 % (P < 0.05) in the EXD group and 18.09-40.95 % in the EX group with no changes in the DI group. In the EXD and DI groups, circulating levels of tumor necrosis factor α and interleukin 6 were decreased after 24 weeks for both groups (P < 0.01). No changes in the EX group. Homeostatic model assessment for insulin resistance decreased (P < 0.05) only after 24 weeks in the EXD group. In AT biopsies, subjects in the EXD and DI groups exhibited a significant decrease in MO (P < 0.01 for all). No changes in AT biopsies were found in the EX group. In conclusion, chronic aerobic exercise was found to have no effects on circulating and AT MOI despite an increased VO2max. Rather important body composition modifications were found to have beneficial effects on circulating and AT MOI in these obese women.

  10. Inflammatory and neurodegeneration markers during asymptomatic HSV-1 reactivation.

    PubMed

    Martin, Carolina; Aguila, Blanca; Araya, Paulina; Vio, Karin; Valdivia, Sharin; Zambrano, Angara; Concha, Margarita I; Otth, Carola

    2014-01-01

    Currently, it is unclear whether asymptomatic recurrent reactivations of herpes simplex virus type 1 (HSV-1) occur in the central nervous systems of infected people, and if these events could lead to a progressive deterioration of neuronal function. In this context, HSV-1 constitutes an important candidate to be included among the risk factors for the development of neuropathies associated with chronic neuroinflammation. The aim of this study was to assess in vivo inflammatory and neurodegenerative markers in the brain during productive and latent HSV-1 infection using a mouse model of herpes simplex encephalitis. Neuroinflammation and neurodegeneration markers were evaluated in mice trigeminal ganglia and cerebral cortex during HSV-1 infection, by immunohistochemistry, western blot, and RT-PCR. Neuronal ICP4 viral antigen expression indicative of a reactivation episode during asymptomatic latency of HSV-1 infection in mice was accompanied by upregulation of neuroinflammatory (toll-like receptor-4, interferon α/β, and p-IRF3) and early neurodegenerative markers (phospho-tau and TauC3). HSV-1 reactivation from latency induced neuroinflammatory and neurodegenerative markers in the brain of asymptomatic mice suggesting that recurrent reactivations could be associated with cumulative neuronal dysfunctions.

  11. Novel inflammatory marker in dialysis patients: YKL-40.

    PubMed

    Okyay, Gülay Ulusal; Er, Ramazan Erdem; Tekbudak, Merve Yasemin; Paşaoğlu, Özge; Inal, Salih; Öneç, Kürşad; Paşaoğlu, Hatice; Altok, Kadriye; Derici, Ülver; Erten, Yasemin

    2013-04-01

    YKL-40 has been introduced as a marker of inflammation in different clinical situations. The association between YKL-40 and inflammation in chronic renal failure patients has not been researched currently. The objectives of this study were to establish serum YKL-40 concentrations in dialysis patients with chronic renal failure compared to healthy subjects and to explore its relationships with a proinflammatory cytokine, interleukine-6 (IL-6) and an acute phase mediator, high sensitivity C-reactive protein (hs-CRP). The study population included hemodialysis patients (N = 43; mean age of 40.9 ± 14.5), peritoneal dialysis patients (N = 38; mean age of 45.8 ± 13.7) and healthy subjects (N = 37; mean age of 45.5 ± 10.6). Serum concentrations of YKL-40, IL-6, hs-CRP and routine laboratory measures were evaluated. Compared to the healthy subjects, hemodialysis and peritoneal dialysis patients had higher concentrations of YKL-40, IL-6, hs-CRP, as well as lower concentrations of hemoglobin, serum albumin and high density lipoprotein-cholesterol (P < 0.001). YKL-40 concentrations were positively correlated with serum creatinine (P < 0.001, r = 0.495), IL-6 (P < 0.001, r = 0.306), hs-CRP (P = 0.001, r = 0.306) levels and inversely correlated with hemoglobin (P = 0.002, r = -0.285), serum albumin (P < 0.001, r = -0.355) and high density lipoprotein-cholesterol (P = 0.001, r = -0.306). In multivariate regression analysis YKL-40 was associated with creatinine, serum albumin and hs-CRP concentrations after adjustments with covariates. Dialysis patients with chronic renal failure have elevated serum YKL-40 concentrations. Associations with standard inflammatory parameters suggest that YKL-40 might be a novel inflammatory marker in this population.

  12. Inflammatory markers in relation to long-term air pollution.

    PubMed

    Mostafavi, Nahid; Vlaanderen, Jelle; Chadeau-Hyam, Marc; Beelen, Rob; Modig, Lars; Palli, Domenico; Bergdahl, Ingvar A; Vineis, Paolo; Hoek, Gerard; Kyrtopoulos, Soterios Α; Vermeulen, Roel

    2015-08-01

    Long-term exposure to ambient air pollution can lead to chronic health effects such as cancer, cardiovascular and respiratory disease. Systemic inflammation has been hypothesized as a putative biological mechanism contributing to these adverse health effects. We evaluated the effect of long-term exposure to air pollution on blood markers of systemic inflammation. We measured a panel of 28 inflammatory markers in peripheral blood samples from 587 individuals that were biobanked as part of a prospective study. Participants were from Varese and Turin (Italy) and Umea (Sweden). Long-term air pollution estimates of nitrogen oxides (NOx) were available from the European Study of Cohorts for Air Pollution Effects (ESCAPE). Linear mixed models adjusted for potential confounders were applied to assess the association between NOx and the markers of inflammation. Long-term exposure to NOx was associated with decreased levels of interleukin (IL)-2, IL-8, IL-10 and tumor necrosis factor-α in Italy, but not in Sweden. NOx exposure levels were considerably lower in Sweden than in Italy (Sweden: median (5th, 95th percentiles) 6.65 μg/m(3) (4.8, 19.7); Italy: median (5th, 95th percentiles) 94.2 μg/m(3) (7.8, 124.5)). Combining data from Italy and Sweden we only observed a significant association between long-term exposure to NOx and decreased levels of circulating IL-8. We observed some indication for perturbations in the inflammatory markers due to long-term exposure to NOx. Effects were stronger in Italy than in Sweden, potentially reflecting the difference in air pollution levels between the two cohorts.

  13. New markers in pelvic inflammatory disease.

    PubMed

    Yang, Shun-Fa; Wu, Tzu-Fan; Tsai, Hsiu-Ting; Lin, Long-Yau; Wang, Po-Hui

    2014-04-20

    Pelvic inflammatory disease (PID) is a common infection in women of reproductive age. However, diagnosis of PID can be difficult due to the wide variation in the symptoms and signs, ranging from subtle or mild symptoms to severe pain in the lower abdomen. Clinical diagnosis alone has only 87% sensitivity and 50% specificity. Therefore, identifying biological factors that are useful for early diagnosis and correlating their expression with the severity of PID could provide significant benefits to women suffering from PID. Pentraxin 3 (PTX3), E-cadherin, myeloperoxidase, stromal cell-derived factor 1 (SDF-1) and the matrix metalloproteinase-9 (MMP-9)/MMP-2 ratio are potential candidates for detecting PID reliably. As PID is often subtle, highly sensitive PID detection methods are needed to promote the prevention of severe sequelae. Growth arrest-specific 6 (Gas6), in combination with its soluble tyrosine kinase receptor, sAxl, could elevate the sensitivity to 92%, which was higher than all other markers tested. Moreover, PTX3, D-dimer and YKL-40 concentrations can predict the clinical course of PID. Although single nucleotide polymorphisms of biomarker genes are not associated with the development of PID, myeloperoxidase SNP -463 G/A and SDF-1 SNP 801 G/A may affect the aggravated expression of their biomarkers in PID. Copyright © 2014. Published by Elsevier B.V.

  14. Effect and Treatment of Chronic Pain in Inflammatory Arthritis

    PubMed Central

    2013-01-01

    Pain is the most common reason patients with inflammatory arthritis see a rheumatologist. Patients consistently rate pain as one of their highest priorities, and pain is the single most important determinant of patient global assessment of disease activity. Although pain is commonly interpreted as a marker of inflammation, the correlation between pain intensity and measures of peripheral inflammation is imperfect. The prevalence of chronic, non-inflammatory pain syndromes such as fibromyalgia is higher among patients with inflammatory arthritis than in the general population. Inflammatory arthritis patients with fibromyalgia have higher measures of disease activity and lower quality of life than inflammatory patients who do not have fibromyalgia. This review article focuses on current literature involving the effects of pain on disease assessment and quality of life for patients with inflammatory arthritis. It also reviews non-pharmacologic and pharmacologic options for treatment of pain for patients with inflammatory arthritis, focusing on the implications of comorbidities and concurrent disease-modifying antirheumatic drug therapy. Although several studies have examined the effects of reducing inflammation for patients with inflammatory arthritis, very few clinical trials have examined the safety and efficacy of treatment directed specifically towards pain pathways. Most studies have been small, have focused on rheumatoid arthritis or mixed populations (e.g., rheumatoid arthritis plus osteoarthritis), and have been at high risk of bias. Larger, longitudinal studies are needed to examine the mechanisms of pain in inflammatory arthritis and to determine the safety and efficacy of analgesic medications in this specific patient population. PMID:23292816

  15. Biologic markers of chronic graft vs. host disease

    PubMed Central

    Pidala, Joseph; Sarwal, Minnie; Roedder, Silke; Lee, Stephanie J.

    2014-01-01

    Biologic markers of chronic graft vs. host disease (GVHD) may provide insight into the pathogenesis of the syndrome, identify molecular targets for novel interventions, and facilitate advances in clinical management. Despite extensive work performed to date largely focused on prediction and diagnosis of the syndrome, little synthesis of findings and validation of promising candidate markers in independent populations has been performed. Studies suggest that risk for subsequent chronic GVHD development may be associated with donor-recipient genetic polymorphism, deficiency in regulatory immune cell populations (NK, Treg, DC2), and variation in inflammatory and immunoregulatory mediators post-HCT (increased TNFα, IL-10 and BAFF, and decreased TGFβ and IL-15). Established chronic GVHD is associated with alteration in immune cell populations (increased CD3+ T cells, Th17, CD4+ and CD8+ effector memory cells, monocytes, CD86 expression, BAFF/B cell ratio, and deficiency of Treg, NK cells, and naïve CD8+ T cells). Inflammatory and immunomodulatory factors (TNFα, IL-6, IL-1β, IL-8, sIL-2R, and IL-1Ra, BAFF, anti-dsDNA, sIL-2Rα, and sCD13) are also perturbed. Little is known about biologic markers of chronic GVHD phenotype and severity, response to therapy, and prognosis. PMID:23872737

  16. [Tumour markers in chronic kidney disease].

    PubMed

    Mercadal, Lucile

    2015-04-01

    Tumour markers are high molecular weight glycoproteins whose interpretation in the presence of chronic renal disease may be disturbed. Apart from the prostate specific antigen, human chorionic gonadotropin and α-fetoprotein, their levels rise with chronic renal failure. For some markers, such as carcinoembryonic antigen, carcinogen antigen (CA) 15-3, cytokeratin fragment 21-1 or calcitonin, a threshold may be defined in a population with chronic renal failure, which may allow their use in cancer surveillance. Others, such as CA125, CA19-9, squamous cell carcinoma and neurospecific enolase, have a high variability and their use in patients with chronic renal disease remains difficult. Copyright © 2015 Association Société de néphrologie. Published by Elsevier SAS. All rights reserved.

  17. Moderate chronic administration of Vineatrol-enriched red wines improves metabolic, oxidative, and inflammatory markers in hamsters fed a high-fat diet.

    PubMed

    Romain, Cindy; Bresciani, Letizia; Gaillet, Sylvie; Feillet-Coudray, Christine; Calani, Luca; Bonafos, Béatrice; Vidé, Joris; Rugani, Nathalie; Ramos, Jeanne; Del Rio, Daniele; Cristol, Jean-Paul; Rouanet, Jean-Max

    2014-06-01

    High-fat (HF) diets contribute to the development of cardiovascular diseases and the metabolic syndrome. This study was undertaken to investigate the beneficial effects of Vineatrol®-enriched red wines on blood lipids, oxidative stress and inflammation, and the role of some metabolic pathway regulatory proteins. Golden Syrian hamsters received an HF diet for 13 wk, in the presence or absence of red wines supplemented with Vineatrol® (RWV) or not. The HF diet increased plasma cholesterol, triglycerides, glucose, and insulin, which were attenuated by RWV treatment. RWV protected against the HF-induced increase in liver nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity and spared antioxidant enzyme activities. RWV did not reduce either liver steatosis or increased plasma leptin due to the HF diet, but greatly improved adiponectinemia. In the liver, RWV affected the inflammatory response by decreasing polymorphonuclear cell number and lowering TNF-α and IL-6 levels. Moreover, the increase in NF-κB activity in the HF group liver was prevented by RWV. Finally, RWV partially corrected low SIRT1 levels due to the HF diet but had no influence on SIRT3 or p-AMPK protein levels. Our studies suggest that RWV is capable of reversing the atherogenic process induced by an HF diet in hamster tissues. © 2014 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

  18. Inflammatory markers and exercise: differences related to exercise type.

    PubMed

    King, Dana E; Carek, Peter; Mainous, Arch G; Pearson, William S

    2003-04-01

    To examine the relationship between elevated inflammatory markers (CRP, fibrinogen, and white blood cell levels) and various forms of exercise for the adult U.S. population while controlling for factors that might influence the relationship. An analysis of the adults age 17 and over who participated in the National Health and Nutrition Examination Survey (NHANES) III was conducted. The main goal of the analysis was to determine whether exercise type was associated with systemic markers of inflammation. Bivariate statistics using chi-square to evaluate different types of exercise according to the presence of elevated and nonelevated inflammatory markers was initially performed. In addition, multivariate models were constructed using each type of exercise activity as the predictor variable and each inflammatory marker as the dependent variable. A total of 4072 people were included in the analysis. In bivariate analyses, compared with nonexercisers in a specific exercise type, a significant lower likelihood of elevated inflammatory markers was found among regular participants in jogging, swimming, cycling, aerobic dancing, calisthenics, and weight lifting but not for gardening. After controlling for possible confounding factors including age, race, sex, body mass index, smoking, and health status in logistic regression analysis, only regular participants in jogging and aerobic dancing remained significantly less likely to have elevated cardiovascular markers. The results of this study indicate that some forms of physical activity are associated with a lower likelihood of elevation of inflammatory markers, although we cannot exclude the possibility that differences may be due to exercise intensity or duration. Future research should be directed toward further exploration of the effects of different types of exercise activity on inflammatory markers and the role of exercise in the prevention of cardiovascular disease.

  19. [Chronic inflammatory demyelinating neuropathies and their variants

    PubMed

    Vallat, J.-M.; Tabaraud, F.; Magy, L.; Macian, F.

    2002-12-01

    The Chronic Inflammatory Demyelinating Polyradiculoneuropathies (CIDP) constitute a syndrome whose incidence is difficult to evaluate, and is probably underestimated. In the course of this presentation, we deliberately restricted discussion to issues raised in recent years concerning the extent of this syndrome. We discuss diagnostic criteria, especially electrophysiological ones. As the criteria proposed by the ad hoc committee of the American Academy of Neurology in 1991 have been questioned due to lack of sensitivity, new ones have been proposed recently. We briefly discuss the different types of chronic dysimmune demyelinating neuropathy: not only the CIDP, but also the Lewis and Sumner syndrome or multifocal inflammatory demyelinating neuropathy and the multiple conduction block neuropathies. At last, we point out the consistent finding of axonal involvement in the course of a chronic demyelinating neuropathy; over time, it can become predominant, which may make diagnosis difficult by suggesting a chronic axonal neuropathy that may be assumed to be primary. Consideration of these points may help clinicians recognize more chronic dysimmune neuropathies, for which immunosuppressive therapy has been found to be effective.

  20. Chronic inflammatory gingival overgrowths: laser gingivectomy & gingivoplasty.

    PubMed

    Shankar, B Shiva; T, Ramadevi; S, Neetha M; Reddy, P Sunil Kumar; Saritha, G; Reddy, J Muralinath

    2013-02-01

    It is quite common to note chronic inflammatory Gingival overgrowths during and/or post orthodontic treatment. Sometimes the overgrowths may even potentially complicate and/or interrupt orthodontic treatment. With the introduction of soft tissue lasers these problems can now be addressed more easily. Amongst many LASERS now available in Dentistry DIODE LASERS seem to be most ideal for orthodontic soft tissue applications. As newer treatments herald into minimally invasive techniques, DIODE LASERS are becoming more promising both in patient satisfaction and dentist satisfaction. How to cite this article: Shankar BS, Ramadevi T, Neetha M S, Reddy P S K, Saritha G, Reddy J M. Chronic Inflammatory Gingival Overgrowths: Laser Gingivectomy & Gingivoplasty. J Int Oral Health 2013; 5(1):83-87.

  1. Chronic Inflammatory Gingival Overgrowths: Laser Gingivectomy & Gingivoplasty

    PubMed Central

    Shankar, B Shiva; T, Ramadevi; S, Neetha M; Reddy, P Sunil Kumar; Saritha, G; Reddy, J Muralinath

    2013-01-01

    It is quite common to note chronic inflammatory Gingival overgrowths during and/or post orthodontic treatment. Sometimes the overgrowths may even potentially complicate and/or interrupt orthodontic treatment. With the introduction of soft tissue lasers these problems can now be addressed more easily. Amongst many LASERS now available in Dentistry DIODE LASERS seem to be most ideal for orthodontic soft tissue applications. As newer treatments herald into minimally invasive techniques, DIODE LASERS are becoming more promising both in patient satisfaction and dentist satisfaction. How to cite this article: Shankar BS, Ramadevi T, Neetha M S, Reddy P S K, Saritha G, Reddy J M. Chronic Inflammatory Gingival Overgrowths: Laser Gingivectomy & Gingivoplasty. J Int Oral Health 2013; 5(1):83-87. PMID:24155582

  2. Emerging Role of Endothelial and Inflammatory Markers in Preeclampsia

    PubMed Central

    Swellam, Menha; Samy, Nervana; Abdl Wahab, Susan; Ibrahim, Mohamed Saeed

    2009-01-01

    Objectives: Endothelial disturbance and excess inflammatory response are pathogenic mechanisms in pre-eclampsia (PE). Authors determine the clinical diagnostic role for thrombomodulin (TM), plasminogen activator inhibitor-1 (PAI-1) as endothelial markers and C-reactive protein (CRP), and interlukin-6 (IL-6) as inflammatory markers when tested independently or in combinations. Materials and methods: We conducted a retrospective study in a cohort of 185 women grouped as 80 women with PE, 55 normotensive pregnant and 50 healthy non-pregnant. Plasma levels of TM, PAI-1, CRP and IL-6 were examined using enzyme linked immunosorbent assays. Results: Median levels and the positivity rates for the investigated markers were higher in PE as compared to the other groups (P < 0.0001). Using linear regression analysis, the investigated markers were significantly correlated regarding healthy nonpregnant vs PE or normotensive pregnant vs PE. The sensitivity of PAI-1 was the highest (98%) among the tested biomarkers. Combination between the investigated markers revealed absolute sensitivity (100%) and reliable specificity especially when PAI-1 was combined with CRP at 83% specificity. Conclusions: Investigated endothelial and inflammatory markers revealed sensitive diagnostic test for PE. However, coupled combination between PAI-1 with CRP showed superior both sensitivity and specificity which represent a promising new approach for detection of PE. PMID:19597295

  3. SHBG, Sex Hormones, and Inflammatory Markers in Older Women

    PubMed Central

    Ceda, Gian Paolo; Lauretani, Fulvio; Bandinelli, Stefania; Corsi, Anna Maria; Giallauria, Francesco; Guralnik, Jack M.; Zuliani, Giovanni; Cattabiani, Chiara; Parrino, Stefano; Ablondi, Fabrizio; Dall'Aglio, Elisabetta; Ceresini, Graziano; Basaria, Shehzad; Ferrucci, Luigi

    2011-01-01

    Context: In premenopausal and older women, high testosterone and estradiol (E2) and low SHBG levels are associated with insulin resistance and diabetes, conditions characterized by low-grade inflammation. Objective: The aim of the study was to examine the relationship between SHBG, total testosterone, total E2, and inflammatory markers in older women. Design and Patients: We conducted a retrospective cross-sectional study of 433 women at least 65 yr old from the InCHIANTI Study, Italy, who were not on hormone replacement therapy or recently hospitalized and who had complete data on SHBG, testosterone, E2, C-reactive protein (CRP), IL-6, soluble IL-6 receptor (sIL-6r), and TNF-α. Relationships between sex hormones and inflammatory markers were examined by multivariate linear regression analyses adjusted for age, body mass index, smoking, insulin, physical activity, and chronic disease. Results: In fully adjusted analyses, SHBG was negatively associated with CRP (P = 0.007), IL-6 (P = 0.008), and sIL-6r (P = 0.02). In addition, testosterone was positively associated with CRP (P = 0.006), IL-6 (P = 0.001), and TNF-α (P = 0.0002). The negative relationship between testosterone and sIL-6r in an age-adjusted model (P = 0.02) was no longer significant in a fully adjusted model (P = 0.12). E2 was positively associated with CRP (P = 0.002) but not with IL-6 in fully adjusted models. In a final model including E2, testosterone, and SHBG, and all the confounders previously considered, SHBG (0.23 ± 0.08; P = 0.006) and E2 (0.21 ± 0.08; P = 0.007), but not testosterone (P = 0.21), were still significantly associated with CRP. Conclusion: In late postmenopausal women not on hormone replacement therapy, SHBG and E2 are, respectively, negative and positive, independent and significant correlates of a proinflammatory state. PMID:21239514

  4. [Immunogenetic HLA markers of chronic viral hepatitis].

    PubMed

    Popov, E A; Levitan, B N; Alekseev, L P; Pronina, O A; Suchkov, S V

    2005-01-01

    To study possible immunogenetic HLA markers of chronic viral hepatitides. Using the reaction of complement-dependent cytotoxicity by Terasaki, we analysed distribution of leukocytic HLA antigens (loci A, B and C) in 179 patients with chronic viral hepatitides B, C and D in Russians and Kazakhs living in the Astrakhan Region. In the Russian population we discovered a significant positive association of CVHB with HLA-B18, HLA-B35, HLA-B40, HLA-Cw3 antigens, and negative one--with HLA-A2. In Kazakhs with CVHB there was a positive association with HLA-A3, HLA-B18 and negative one--with HLA-A11. Alleles HLA-A10, HLA-B35, HLA-B40 and HLA-Cw3 mark CVHC in Russians. HLA-Cw4 specificity acts as protector in development of chronic HCV-infection. A correlation was found between carriage of some specificities and haplotypes of HLA and activity of chronic HBV and HCV infection. A high risk of chronic delta infection in Russians is associated with HLA-B8 and HLA-B35, in Kazakhs--with HLA-B35 and HLA-D40. There are significant associations between CVHB, CVHC, chronic delta infection and some HLA haplotypes. A universal role of HLA-B35 specificity in development of CVH irrespective of hepatotropic virus and patients' nationality is shown.

  5. Maternal inflammatory markers and term labor performance.

    PubMed

    Cierny, Jill T; Unal, E Ramsey; Flood, Pamela; Rhee, Ka Young; Praktish, Allison; Olson, Tara Hudak; Goetzl, Laura

    2014-05-01

    We sought to examine the relationship between maternal markers of inflammation and labor performance. A nested cohort study was performed utilizing an established cohort of term nulliparous patients. Maternal blood was collected at the onset of regular, painful contractions in patients undergoing labor induction or at admission in patients with spontaneous labor. Levels of cytokines including interleukin (IL)-1, IL-6, and tumor necrosis factor-α were determined using standard multiplex methodology. Maternal demographic data were collected prospectively. Detailed retrospective chart review was performed to extract data on cervical dilation, effacement, and station during labor. Subjects were excluded if they failed to achieve complete dilation. Mixed effects modeling was used to examine the association between serum cytokine quartiles and labor progress in the latent and active phases. In all, 334 women were included in our analysis. The lowest quartile of IL-6 was associated with slower latent labor (P = .001). In contrast, the highest quartiles of IL-1 and tumor necrosis factor-α were associated with slower active labor (P = .03 and .0002, respectively). Proinflammatory activation is important in labor initiation. However, once active labor is established, excess inflammation can be detrimental to efficient labor progress. These data may explain, in part, the known associations among clinical chorioamnionitis, cesarean delivery, and postpartum hemorrhage. Copyright © 2014 Mosby, Inc. All rights reserved.

  6. Noninvasive Markers of Disease Activity in Inflammatory Bowel Disease

    PubMed Central

    Kane, Sunanda

    2014-01-01

    It is often difficult to assess disease activity in inflammatory bowel disease (IBD). Noninvasive biomarkers are a means of quantifying often nebulous symptoms without subjecting patients to endoscopy or radiation. This paper highlights markers present in feces, serum, or urine that have all been compared with the gold standard, histologic analysis of endoscopically collected specimens. Two categories of markers are featured: well-researched markers of mucosal inflammation with high sensitivity and specificity (calprotectin, lactoferrin, and S100A12) and novel promising markers, some of which are already clinically employed for reasons unrelated to IBD (interleukin [IL]-17, IL-33/ST2, adenosine deaminase, polymorphonuclear elastase, matrix metalloproteinase-9, neopterin, serum M30, and fecal immunohistochemistry). The data pertaining to the more-established markers are intended to highlight recent clinical applications for these markers (ie, assessing disease outside of the colon or in the pediatric population as well as being a cost-saving alternative to colonoscopy to screen for IBD). As there is no evidence to date that a specific marker will accurately be able to represent the entire IBD patient population, it is likely that a combination of the existing markers will be most clinically relevant to the practicing gastroenterologist attempting to evaluate disease severity in a specific patient. Familiarity with the most promising emerging markers will allow a better understanding of new studies and their impact on patient care. PMID:27551251

  7. Resistin as an inflammatory marker in patients with schizophrenia treated with clozapine.

    PubMed

    Klemettilä, Jari-Pekka; Kampman, Olli; Seppälä, Niko; Viikki, Merja; Hämäläinen, Mari; Moilanen, Eeva; Leinonen, Esa

    2017-02-01

    Schizophrenia is associated with excess cardiovascular comorbidity and mortality related to lifestyle factors, such as lack of physical activity, poor diet, and smoking. The prevalence of metabolic syndrome is increased among patients with schizophrenia, with the highest rates among patients on clozapine treatment. Smoking, obesity, physical inactivity, airway inflammation and obstruction, and adipose tissue and inflammatory marker activation are related in systemic inflammation. Low-grade inflammation is also associated with schizophrenia. Adipokine resistin is a biomarker involving several acute and chronic inflammatory states. However, the inflammatory role of resistin is so far inconclusive and studies in schizophrenia are scanty. The aim of the present study was to explore the role of serum resistin as an inflammatory marker in patients with schizophrenia on clozapine treatment. Associations between serum levels of resistin and some other selected cytokines/adipokines (adiponectin, leptin, adipsin, IL-6, IL-1Ra, TNF-α, hs-CRP) and metabolic markers in 190 patients with schizophrenia on clozapine treatment were studied using a cross-sectional study design. Among male patients especially, smokers had higher levels of resistin than non-smokers, and among smokers resistin levels were associated with IL-1Ra and hs-CRP levels. In the whole patient group levels of resistin associated with levels of IL-1Ra, and among male patients with low HDL-cholesterol. Resistin is a biomarker of systemic inflammation associated with smoking among patients with schizophrenia on clozapine treatment. Resistin might have a role as a marker of cardiovascular comorbidity.

  8. Cocoa Polyphenols and Inflammatory Markers of Cardiovascular Disease

    PubMed Central

    Khan, Nasiruddin; Khymenets, Olha; Urpí-Sardà, Mireia; Tulipani, Sara; Garcia-Aloy, Mar; Monagas, María; Mora-Cubillos, Ximena; Llorach, Rafael; Andres-Lacueva, Cristina

    2014-01-01

    Epidemiological studies have demonstrated the beneficial effect of plant-derived food intake in reducing the risk of cardiovascular disease (CVD). The potential bioactivity of cocoa and its polyphenolic components in modulating cardiovascular health is now being studied worldwide and continues to grow at a rapid pace. In fact, the high polyphenol content of cocoa is of particular interest from the nutritional and pharmacological viewpoints. Cocoa polyphenols are shown to possess a range of cardiovascular-protective properties, and can play a meaningful role through modulating different inflammatory markers involved in atherosclerosis. Accumulated evidence on related anti-inflammatory effects of cocoa polyphenols is summarized in the present review. PMID:24566441

  9. Serological markers in inflammatory bowel disease: the pros and cons.

    PubMed

    Lerner, Aaron; Shoenfeld, Yehuda

    2002-02-01

    Accurate serological assays are desirable for the diagnosis of inflammatory bowel disease. Among several serological markers anti-Saccharomyces cerevisiae mannan antibodies and perinuclear antineutrophil cytoplasmic autoantibodies are highly disease specific for Crohn's disease and ulcerative colitis, respectively. Combining the two improves their specificity. Sensitivity, however, is still low. Due to lack of standardization and vast interobserver variability, they cannot be used as the only diagnostic criteria but can assist clinicians in diagnosing and categorizing patients with inflammatory bowel disease as well as in helping them to take therapeutic decisions.

  10. Lipoprotein redox status evaluation as a marker of cardiovascular disease risk in patients with inflammatory disease

    PubMed Central

    Ungurianu, Anca; Margină, Denisa; Grădinaru, Daniela; Băcanu, Claudia; Ilie, Mihaela; Tsitsimpikou, Christina; Tsarouhas, Konstantinos; Spandidos, Demetrios A.; Tsatsakis, Aristides M.

    2016-01-01

    Patients with chronic inflammatory disorders (ID) have an increased risk of developing cardiovascular disease, and routinely determined parameters do not reveal the real metabolic status of specific subgroups, such as patients with rheumatoid arthritis (RA). In this study, in order to evaluate state of the art markers for the assessment of cardiometabolic risk, abnormalities in lipoprotein levels in patients with a low-grade inflammatory status [diabetes mellitus (DM) subgroup] and in patients with a high systemic inflammatory burden (RA subgroup) was determined. The study group comprised patients with ID [DM (n=20) and RA (n=20)], with an aged-matched control group (n=17). Patient serum was used to determine routine biochemical parameters and to isolate low-density lipoprotein (LDL) and high-density lipoprotein (HDL). The heparin-citrate method was used for LDL precipitation and the phosphotungstic acid-MgCl2 technique for the isolation of HDL. Further, Amplex Red and advanced oxidation protein product (AOPP) assays were applied to determine lipid peroxides and protein oxidation, respectively, while the levels of serum advanced glycation end products (AGEs) were also determined. Although the differences in the routinely determined lipidemic profile were notable between the DM and RA subgroups, markers of lipid peroxidation and of advanced protein oxidation/glycation did not differ significantly, indicating possible similar oxidative damage of serum lipoproteins. On the whole, as alterations in lipoprotein functionality can occur long before any changes in routinely measured biochemical parameters are observed, more sensitive markers for the assessment of cardiovascular risk are required. As AOPPs, AGEs, oxidized LDL (oxLDL) and especially oxidized HDL (oxHDL) are affected during the early stages of inflammatory disease, and due to their known link to coronary artery disease, it would be wise to include these markers in the routine cardiovascular evaluation of

  11. [Use of inflammatory markers for monitoring paediatric asthma].

    PubMed

    Vidal G, Alberto

    2015-01-01

    The assessment of asthma control takes into account the symptoms, quality of life, lung function, and inflammatory markers. In the last few years, there has been a large increase in the number of publications related to the study of biomarkers in the management of paediatric asthma. Despite the large variety of inflammatory markers described in research studies, only a small group has shown to be useful in monitoring the disease. Induced sputum eosinophils offer the most solid evidence in assessing asthma control. Exhaled breath condensate and urinary leucotrienes could be useful in the future if there is standardisation in their procedures and interpretation of the results. Nitric oxide, basic eosinophil cationic protein, and bronchial biopsy with bronchoalveolar lavage, only appeared to be useful in a reduced group of patients. Copyright © 2015 Sociedad Chilena de Pediatría. Publicado por Elsevier España, S.L.U. All rights reserved.

  12. Detection of Periodontal Markers in Chronic Periodontitis

    PubMed Central

    Leonhardt, Åsa; Carlén, Anette; Bengtsson, Lisbeth; Dahlén, Gunnar

    2011-01-01

    The aim was to compare the detection frequency of periodontopathogens by using the Pado Test 4.5 and checkerboard DNA-DNA hybridization technique in chronic periodontitis patients. Thirty patients with chronic periodontitis were tested cross-sectionally with DNA/RNA oligogenomic probe method (IAI Pado Test 4.5) and DNA/DNA whole genomic probe (checkerboard) method. Samples were taken by two paper points at the deepest site in each of the four quadrants and pooled into one sample for each of the two methods. The samples were sent to the two laboratories (IAI, Zuchwil, Switzerland, and Oral Microbiology Laboratory, University of Gothenburg, Sweden) and were analyzed in a routine setting for the presence and amount of Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Tannerella forsythia and Treponema denticola. While Pado Test 4.5 detected the four periodontal pathogens in 11 (36.7%) of the patients, the checkerboard method showed presence in all patients (100%) using the lower score (Score 1 corresponding to 104 bacterial cells) and 16 (53.3%) using a higher treshold (score 3 corresponding to between >105 and 106 cells). The results of the present study showed low agreement for a positive microbiological outcome using the two diagnostic methods. It was also concluded that microbiological analysis in practice should include a larger number of bacterial species to better serve as markers for a diseased associated flora in chronic periodontitis cases. PMID:21769304

  13. A critical evaluation of inflammatory markers in Huntington's Disease plasma.

    PubMed

    Silajdžić, Edina; Rezeli, Melinda; Végvári, Ákos; Lahiri, Nayana; Andre, Ralph; Magnusson-Lind, Anna; Nambron, Rajasree; Kalliolia, Eirini; Marko-Varga, György; Warner, Thomas T; Laurell, Thomas; Tabrizi, Sarah J; Björkqvist, Maria

    2013-01-01

    Huntington's Disease (HD) is a hereditary, progressive neurodegenerative disorder characterised by both neurological and systemic symptoms. In HD, immune changes can be observed before the onset of overt clinical features raising the possibility that inflammatory markers in plasma could be used to track disease progression. It has previously been demonstrated that a widespread, progressive innate immune response is detectable in plasma throughout the course of HD. The aim of the present study was to investigate the potential of several components of inflammation and innate immunity as plasma biomarkers in HD. We utilised antibody-based detection technologies as well as mass spectrometric quantification, multiple reaction monitoring (MRM-MS). Levels of several markers previously described as altered in HD, such as clusterin, complement component 4, complement component 9 and α-2 macroglobulin did not differ between healthy controls and HD subjects as measured by Luminex, ELISA or MRM-MS. C-reactive protein was decreased in early HD, while the other immune markers tested were unaltered. Although only C-reactive protein was found to be reduced in early HD, some of the inflammatory markers measured correlated with clinical measures.

  14. Inflammatory markers in SIRS, sepsis and septic shock.

    PubMed

    Herzum, I; Renz, H

    2008-01-01

    Despite great advancement in the understanding of the pathophysiology and in the development of novel therapeutic approaches, mortality of sepsis still remains unacceptably high. Adequate laboratory diagnostics represents a major requirement for the improvement of this situation. For a better understanding of the immunological dysregulation in this disease, several markers are now available for routine diagnostics in the clinical laboratory. They include the cytokines interleukin (IL) -6, IL-8, procalcitonin and the LPS-binding protein (LBP). These novel markers will be compared to the conventional procedure of diagnosing inflammatory and infectious disease, such as measurements of C-reactive protein (CRP) as a major acute phase protein and differential blood counting. Important questions addressed in this review are the usefulness of these markers for early diagnosis, their role as prognostic markers and in the risk assessment of patients. Furthermore, we will discuss whether these parameters are to differentiate between systemic inflammatory response syndrome (SIRS) and sepsis at its different degrees. In the case of an infectious nature of the disease, it is important to differentiate between viral or bacterial origin and to monitor the responsiveness of antibiotic therapies. The literature was analysed with focus on the evidence for diagnostic and analytical performance. For this purpose international definition and staging criteria were used in context of criteria for assay performance including sensitivity, specificity, negative and positive predictive values, ROC analysis and other analytical criteria.

  15. Pancreatic function in chronic inflammatory bowel disease.

    PubMed

    Angelini, G; Cavallini, G; Bovo, P; Brocco, G; Castagnini, A; Lavarini, E; Merigo, F; Tallon, N; Scuro, L A

    1988-03-01

    This study was prospectively carried out to evaluate the frequency and clinical significance of pancreatic impairment in the course of chronic inflammatory bowel disease (CIBD). Twenty-seven patients affected by ulcerative colitis or Crohn's disease were submitted to a secretin-cerulein test, oral glucose test (OGT) and to indirect immunofluorescence (IFL) for detection of autoantibodies against exocrine and endocrine tissue. A bicarbonate plus enzyme or only an enzyme insufficiency was found in 11/27 patients, whereas isolated lipase decrease was observed in 18 subjects. In the results of the OGT and the indirect IFL test there was no difference between patients and controls. These data demonstrate that pancreatic impairment is a far more frequent occurrence than generally recognized in clinical practice. The decrease of lipase secretion could worsen the consequences of malabsorption in Crohn's disease of the small intestine. Therefore we think that a pancreatic assessment is advisable, at least in Crohn's disease patients with steatorrhea.

  16. [Pathogenesis of chronic inflammatory demyelinating polyneuropathy].

    PubMed

    Aranami, Toshimasa; Yamamura, Takashi

    2013-05-01

    Chronic inflammatory demyelinating polyneuropathy (CIDP) is considered to be a demyelinating autoimmune disorder in the peripheral nervous system. Concerning cellular immune response, activity of IFN-gamma producing Th1 and IL-17 producing Th17 cells might be accelerated in patients with CIDP, while regulatory function of CD4+ CD25(high) Foxp3+ regulatory T cells might be diminished. Humoral immune responses against several myelin components such as myelin protein zero and gangliosides such as GM1 might be also induced in a part of patients with CIDP. Besides, growing body of evidences suggest that immune response against several molecules expressed in the noncompact myelin might be involved in the pathogenesis of CIDP.

  17. Chronic inflammatory demyelinating polyradiculoneuropathy with cholesterol deposits in a dog.

    PubMed

    Piñeyro, Pablo; Sponenberg, D Philip; Pancotto, Theresa; King, Rosalind H M; Jortner, Bernard S

    2015-11-01

    Chronic inflammatory demyelinating polyradiculoneuropathy occurred in an 11-year-old Labrador Retriever dog. Spinal cord compression resulted from massive radiculitis with prominent cholesterol granulomas. Cholesterol deposition and associated granuloma formation is unique in chronic inflammatory demyelinating polyradiculoneuropathy, in both its human and canine expressions. © 2015 The Author(s).

  18. Gender differences in fat distribution and inflammatory markers among Arabs.

    PubMed

    Farooq, Abdulaziz; Knez, Wade L; Knez, Kelly; Al-Noaimi, Asma; Grantham, Justin; Mohamed-Ali, Vidya

    2013-01-01

    Recent studies from the Gulf region suggest that compared to men, women have a greater risk of developing metabolic syndrome (MeS). To investigate gender differences in body composition, adipokines, inflammatory markers, and aerobic fitness in a cohort of healthy Qatari adults. Participants. Healthy Qatari (n = 58) were matched for age, gender, and body mass index. Body composition and regional fat distribution were determined by dual-energy X-ray absorptiometry and computerized tomography. Laboratory assessments included serum levels of fasting glucose, insulin, lipid profile analysis, adipokines, and inflammatory markers. Subjects were also evaluated for aerobic fitness. Women had more adipose tissue in the total abdominal (P = 0.04) and abdominal subcutaneous (P = 0.07) regions compared to men. Waist circumference and indices of insulin sensitivity were similar; however, women had a more favourable lipid profile than men. Serum adiponectin and leptin levels were significantly higher in women, whereas inflammatory profiles were not different between men and women. Aerobic fitness was lower in women and was associated with abdominal fat accumulation. In premenopausal women, higher levels of adiponectin may support maintenance of insulin sensitivity and normolipidemia despite greater adiposity. However, poor aerobic fitness combined with abdominal fat accumulation may explain their greater future risk of MeS compared with men.

  19. Inflammatory and immunogenetic markers in correlation with pulmonary tuberculosis*

    PubMed Central

    Muller, Beatriz Lima Alezio; Ramalho, Daniela Maria de Paula; dos Santos, Paula Fernanda Gonçalves; Mesquita, Eliene Denites Duarte; Kritski, Afranio Lineu; Oliveira, Martha Maria

    2013-01-01

    OBJECTIVE: To describe serum levels of the cytokines IL-10, TNF-α, and IFN-γ, as well as polymorphisms in the genes involved in their transcription, and their association with markers of the acute inflammatory response in patients with pulmonary tuberculosis. METHODS: This was a descriptive, longitudinal study involving 81 patients with pulmonary tuberculosis treated at two referral hospitals. We collected data on sociodemographic variables and evaluated bacteriological conversion at the eighth week of antituberculosis treatment, gene polymorphisms related to the cytokines studied, and serum levels of those cytokines, as well as those of C-reactive protein (CRP). We also determined the ESR and CD4+ counts. RESULTS: The median age of the patients was 43 years; 67 patients (82.7%) were male; and 8 patients (9.9%) were infected with HIV. The ESR was highest in the patients with high IFN-γ levels and low IL-10 levels. IFN-γ and TNF-α gene polymorphisms at positions +874 and −238, respectively, showed no correlations with the corresponding cytokine serum levels. Low IL-10 levels were associated with IL-10 gene polymorphisms at positions −592 and −819 (but not −1082). There was a negative association between bacteriological conversion at the eighth week of treatment and CRP levels. CONCLUSIONS: Our results suggest that genetic markers and markers of acute inflammatory response are useful in predicting the response to antituberculosis treatment. PMID:24473766

  20. Buprenorphine Alters Inflammatory and Oxidative Stress Molecular Markers in Arthritis

    PubMed Central

    Hitchon, Carol

    2017-01-01

    Buprenorphine is recommended for use as an analgesic in animal models including in murine models of collagen-induced arthritis (CIA). However, the effect of buprenorphine on the expression of disease-associated biomarkers is not well defined. We examined the effect of buprenorphine administration on disease progression and the expression of inflammatory and oxidative stress markers, in a murine model of CIA. Buprenorphine administration altered the expression of cytokines, IFN-γ, IL-6, and MMP-3, and oxidative markers, for example, iNOS, superoxide dismutase (SOD1), and catalase (CAT), in the CIA mice. As buprenorphine is an analgesic, we further monitored the association of expression of these biomarkers with pain scores in a human cohort of early rheumatoid arthritis (RA). Serum MMP-3 levels and blood mRNA expression of antioxidants sod1 and cat correlated with pain scores in the RA cohort. We have demonstrated that administration of buprenorphine alters the expression of inflammatory and oxidative stress-related molecular markers in a murine model of CIA. This caveat needs to be considered in animal experiments using buprenorphine as an analgesic, as it can be a confounding factor in murine studies used for prediction of response to therapy. Furthermore, the antioxidant enzymes that showed an association with pain scores in the human cohort may be explored as biomarkers for pain in future studies. PMID:28572711

  1. Septic versus inflammatory arthritis: discriminating the ability of serum inflammatory markers.

    PubMed

    Talebi-Taher, Mahshid; Shirani, Fatemeh; Nikanjam, Najmeh; Shekarabi, Mehdi

    2013-02-01

    Early diagnosis of septic arthritis is very important. Few studies showed diagnostic accuracy of serum inflammatory markers in septic arthritis. The aim of our study was to compare the serum and synovial fluid markers [procalcitonin, serum IL-6, TNF-α, C-reactive protein, erythrocyte sedimentation rate, synovial fluid white blood cell counts and PMN percentage] in septic and inflammatory arthritis. Seventy-five patients, including 25 and 50 septic and non-septic arthritis, were enrolled in the study. The serum and synovial fluid markers [procalcitonin, serum IL-6, TNF-α, C-reactive protein, erythrocyte sedimentation rate, synovial fluid white blood cell counts, and PMN percentage] were compared in septic and inflammatory arthritis. Patients with septic arthritis had significantly elevated levels of procalcitonin, serum TNF-α, C-reactive protein, erythrocyte sedimentation rate, synovial fluid white blood cell counts, and PMN percentage in comparison with the inflammatory arthritis group (P < 0.00). Serum IL-6 level does not differ among the two groups. In a receiver operating characteristic curve analysis, synovial fluid WBC counts, PMN percentage, TNF-α, ESR, and serum PCT preformed best in distinguishing between septic and non-septic arthritis. Our study suggests that PCT can be used to diagnose the septic arthritis, but more studies warranted in order to determine the specificity and sensitivity of the test.

  2. Duration of red blood cell storage and inflammatory marker generation

    PubMed Central

    Sut, Caroline; Tariket, Sofiane; Chou, Ming Li; Garraud, Olivier; Laradi, Sandrine; Hamzeh-Cognasse, Hind; Seghatchian, Jerard; Burnouf, Thierry; Cognasse, Fabrice

    2017-01-01

    Red blood cell (RBC) transfusion is a life-saving treatment for several pathologies. RBCs for transfusion are stored refrigerated in a preservative solution, which extends their shelf-life for up to 42 days. During storage, the RBCs endure abundant physicochemical changes, named RBC storage lesions, which affect the overall quality standard, the functional integrity and in vivo survival of the transfused RBCs. Some of the changes occurring in the early stages of the storage period (for approximately two weeks) are reversible but become irreversible later on as the storage is extended. In this review, we aim to decipher the duration of RBC storage and inflammatory marker generation. This phenomenon is included as one of the causes of transfusion-related immunomodulation (TRIM), an emerging concept developed to potentially elucidate numerous clinical observations that suggest that RBC transfusion is associated with increased inflammatory events or effects with clinical consequence. PMID:28263172

  3. Metabolic Syndrome and Selective Inflammatory Markers in Psoriatic Patients

    PubMed Central

    Vachatova, Simona; Andrys, Ctirad; Salavec, Miloslav; Ettler, Karel; Rehacek, Vit; Cermakova, Eva; Malkova, Andrea

    2016-01-01

    The presented article studies the role of selected inflammatory and anti-inflammatory serum markers of psoriatic patients in the pathogenesis of metabolic syndrome (MS) and psoriasis. The study is based on the comparison between the group of psoriatic patients (74) and the control group (65). We found significantly higher BMI (p < 0.05) and diastolic blood pressure (p < 0.05) in the psoriatic patients. The values of waist circumference and BMI were significantly higher (p < 0.05) in the male patients compared to the men in the control group. The analysis revealed significantly higher CRP (p < 0.001), Lp-PLA2 (p < 0.001), leptin (p < 0.01), and resistin (p < 0.01) levels in the psoriatic patients. Significantly higher levels of CRP (p < 0.01), Lp-PLA2 (p < 0.001), leptin (p < 0.01), and resistin (p < 0.05) were found in the patients with MS compared to the controls with MS. The level of adiponectin was significantly lower (p < 0.01) in the patients with MS. Finally, we found significantly higher level of Lp-PLA2 (p < 0.001) in the group of patients without MS compared to the controls without MS. In conclusion, observed inflammatory and anti-inflammatory markers (CRP, adiponectin, leptin, resistin, and Lp-PLA2) are involved in both pathogenesis of MS and pathogenesis of psoriasis. The level of Lp-PLA2 indicates the presence of subclinical atherosclerosis (cardiovascular risk) in psoriatic patients. PMID:28097156

  4. Immune-inflammatory markers in massively disseminated cysticercosis.

    PubMed

    Panda, Akhila Kumar; Pati, Binod Kumar

    2014-04-09

    Disseminated cysticercosis is a common endemic tropical infection. We report a 24-year-old man who presented with a single episode of focal seizure and transient depression. Imaging studies revealed disseminated vesicular cysticercosis involving almost all the body parts. In spite of severe dissemination and significantly raised immunological inflammatory markers, the patient had negligible symptoms. He was subsequently followed up with oral corticosteroid and antiepileptic drug without further complication. The extensive dissemination, relatively benign nature of the disease and clinicoradiological discordance are interesting to describe. This neglected tropical infection can sometimes be alarming and needs public health awareness.

  5. Changes in Inflammatory and Bone Turnover Markers After Periodontal Disease Treatment in Patients With Diabetes.

    PubMed

    Izuora, Kenneth E; Ezeanolue, Echezona E; Neubauer, Michael F; Gewelber, Civon L; Allenback, Gayle L; Shan, Guogen; Umpierrez, Guillermo E

    2016-06-01

    The underlying mechanisms for increased osteopenia and fracture rates in patients with diabetes are not well understood, but may relate to chronic systemic inflammation. We assessed the effect of treating periodontal disease (POD), a cause of chronic inflammation, on inflammatory and bone turnover markers in patients with diabetes. Using an investigator-administered questionnaire, we screened a cross-section of patients presenting for routine outpatient diabetes care. We recruited 22 subjects with POD. Inflammatory and bone turnover markers were measured at baseline and 3 months following POD treatment (scaling, root planing and subantimicrobial dose doxycycline). There were nonsignificant reductions in high-sensitivity C-reactive protein (6.34-5.52mg/L, P = 0.626) and tumor necrosis factor-alpha (10.37-10.01pg/mL, P = 0.617). There were nonsignificant increases in urinary C-terminal telopeptide (85.50-90.23pg/mL, P = 0.684) and bone-specific alkaline phosphatase (7.45-8.79pg/mL, P = 0.074). Patients with >90% adherence with doxycycline were 6.4 times more likely to experience reduction in tumor necrosis factor-alpha (P = 0.021) and 2.8 times more likely to experience reductions in high-sensitivity C-reactive protein (P = 0.133). Treatment of POD in patients with diabetes resulted in nonsignificant lowering of inflammatory markers and nonsignificant increase in bone turnover markers. However, adherence to doxycycline therapy resulted in better treatment effects. Copyright © 2016 Southern Society for Clinical Investigation. Published by Elsevier Inc. All rights reserved.

  6. Treatment of chronic inflammatory demyelinating polyneuropathy.

    PubMed

    Kleyman, Inna; Brannagan, Thomas H

    2015-07-01

    Chronic inflammatory demyelinating polyneuropathy (CIDP) is one of the acquired demyelinating neuropathies and is considered to be immune mediated. Diagnosis is typically based on clinical history, neurologic examination, electrophysiologic studies, CSF studies, and pathologic examination. Early diagnosis and treatment is important to prevent irreversible axonal loss and optimize improvement in function. The first-line agents for treatment are intravenous immunoglobulin (IVIg), corticosteroids, and plasmapheresis, which have all been demonstrated to be effective in controlled studies. Studies have not shown a significant difference between these three treatments, and the initial choice of therapy is often based on availability, cost, ease of administration, and side effect profile. If patients do not respond to one of these agents, they may respond to one of the others and sometimes in combination. If the first-line agents are not effective, chemotherapeutic or immunosuppressive agents may be considered. There are limited controlled studies of these modalities, and they are often used in conjunction with a first-line treatment. The majority of patients require long-term therapy to maintain a response and to prevent relapse.

  7. Therapeutic options for chronic inflammatory demyelinating polyradiculoneuropathy: a systematic review

    PubMed Central

    2014-01-01

    Background Chronic inflammatory demyelinating polyradiculoneuropathy is a rare acquired immune-mediated progressive or relapsing disorder causing peripheral neuropathic disease of duration more than two months. Many individuals with chronic inflammatory demyelinating polyradiculoneuropathy fail to make a long-term recovery with current treatment regimes. The aim of this study was to prospectively review the literature to determine the effectiveness of therapies for chronic inflammatory demyelinating polyradiculoneuropathy. Methods Articles published from January 1990 to December 2012 were searched for studies to treat adults with chronic inflammatory demyelinating polyradiculoneuropathy. Peer-reviewed full-text articles published in English were included. Results Nine placebo-controlled double-blinded randomised trials were reviewed to treat subjects with chronic inflammatory demyelinating polyradiculoneuropathy exhibiting various degrees of effectiveness. The most effect treatments were; three randomised controlled trials using intravenous immunoglobulin, a study comparing pulsed dexamethasone and short term prednisolone and rituximab all showed promising results and were well tolerated. Conclusion IVIg and corticosteroids remain first line treatments for CIDP. Therapies using monoclonal antibodies, such as Rituximab and Natalizumab offer the most promise for treatment of Chronic inflammatory demyelinating polyradiculoneuropathy however they also need further research, as does the use of stem cell therapy for treating Chronic inflammatory demyelinating polyradiculoneuropathy. Large randomised controlled trials and better patient selection are required to address responsiveness of CIDP patients to conventional treatments to elucidate mechanisms of action and future directions for therapeutic improvement. PMID:24507546

  8. Inflammatory and Oxidative Stress Markers in Experimental Allergic Asthma.

    PubMed

    Nesi, Renata Tiscoski; Kennedy-Feitosa, Emanuel; Lanzetti, Manuella; Ávila, Mariana Barcellos; Magalhães, Clarissa Bichara; Zin, Walter Araújo; Faffe, Débora Souza; Porto, Luís Cristóvão; Valença, Samuel Santos

    2017-08-01

    Ovalbumin-induced allergic lung inflammation (ALI) is a condition believed to be mediated by cytokines, extracellular matrix remodeling, and redox imbalance. In this study, we evaluated pulmonary function together with inflammatory markers as interleukin-4 (IL-4), myeloperoxidase (MPO), eosinophil cells, and redox markers in the lungs of BALB/c mice after ovalbumin (OVA) sensitization and challenge. Our results showed an increase in bronchial hyperresponsiveness stimulated by methacholine (Mch), inflammatory cell influx, especially eosinophils together with an increase of high mobility group box 1 (HMGB1) and altered lipid peroxidation (LP) and antioxidant defenses in the OVA group compared to the control group (p ≤ 0.5). Thus, we demonstrated that OVA-induced ALI altered redox status concomitantly with impaired lung function, which was associated with HMGB1 expression and proteolytic remodeling. Taken together all results found here, we may suggest HMGB1 is an important therapeutic target for asthma, once orchestrates the redox signaling, inflammation, and remodeling that contribute to the disease development.

  9. Maternal diet, gestational weight gain, and inflammatory markers during pregnancy.

    PubMed

    Hrolfsdottir, Laufey; Schalkwijk, Casper G; Birgisdottir, Bryndis E; Gunnarsdottir, Ingibjorg; Maslova, Ekaterina; Granström, Charlotta; Strøm, Marin; Olsen, Sjurdur F; Halldorsson, Thorhallur I

    2016-10-01

    To examine the associations of gestational weight gain (GWG) and diet with low-grade inflammation in pregnancy. A cross-sectional analysis of 671 pregnant women was performed, and diet was assessed in gestational week 30. GWG was recorded in weeks 30 and ∼37 (difference between the weight recorded at these time points and pre-pregnancy weight). Markers of inflammation, high-sensitivity C-reactive protein (hsCRP), serum amyloid A (SAA), interleukin (IL)-6, IL-8, IL-1β, and tumor necrosis factor-α were quantified in serum from week 30. After adjusting for age, pre-pregnancy BMI, parity, smoking status, and education, each 1 kg increase in GWG was associated with 3% (95% CI: 1-5) higher hsCRP and 3% (95% CI: 1-4) higher SAA concentrations, which corresponded to ∼18% to 25% increase in these biomarkers among those with excessive weight gain. GWG was inversely associated with IL-8 while no associations were found for the other inflammatory markers. With respect to diet, women in the highest compared with lowest quintile of protein intake had 26% (95% CI: 3-54) higher hsCRP concentrations. This increase appeared to be driven by intake of animal protein. A similar pattern was observed for SAA. Excessive GWG, as well as high intake of animal protein, was associated with higher concentrations of inflammatory factors. © 2016 The Obesity Society.

  10. Effect of zinc supplementation on inflammatory markers and adipokines in young obese women.

    PubMed

    Kim, Jihye; Ahn, Juhee

    2014-02-01

    Obesity is a chronic inflammatory state characterized by altered adipokine production and increased levels of inflammatory cytokines. The study explored the effect of zinc supplementation on inflammatory markers and adipocyte hormones in young obese women. Twenty five non-obese women and forty obese women (body mass index ≥25 kg/m(2)) aged 19-28 years were recruited for this study. Twenty obese women of the study group took 30 mg/day of supplemental zinc as zinc gluconate for 8 weeks and 20 obese women of control group took placebo. Usual dietary zinc intake was estimated from 3-day diet records. Serum zinc and urinary zinc concentration were measured by Atomic Absorption Spectrophotometry. Inflammatory markers such as high sensitivity C-reactive protein (hs-CRP), tumor necrosis factor-alpha (TNF-α), and interleukin (IL)-6 and adipocyte hormones such as lepin and adiponectin were measured by enzyme immunoassay. Inflammatory markers and leptin were significantly higher, but adiponectin was significantly lower in obese women than non-obese women. Zinc supplementation increased serum zinc by 15% and urinary zinc by 56% (P < 0.05). The levels of hs-CRP (P = 0.03) and IL-6 (P = 0.006) significantly decreased with zinc supplementation, but not in placebo group. Serum leptin and plasma adiponectin concentration did not differ with either zinc supplementation or placebo. The levels of IL-6 and leptin were inversely associated with dietary zinc intake. These results suggest that zinc may have a favorable effect on obesity-related inflammation in young adults.

  11. The alteration of zinc transporter gene expression is associated with inflammatory markers in obese women.

    PubMed

    Noh, Hwayoung; Paik, Hee Young; Kim, Jihye; Chung, Jayong

    2014-04-01

    Obesity, a chronic inflammatory state, is associated with altered zinc metabolism. ZnT and Zip transporters are involved in the regulation of zinc metabolism. This study examined the relationships among obesity, zinc transporter gene expression, and inflammatory markers in young Korean women. The messenger RNA (mRNA) levels of leukocyte zinc transporters between obese (BMI = 28.3 ± 0.5 kg/m(2), n = 35) and nonobese (BMI = 20.7 ± 0.2 kg/m(2), n = 20) women aged 18-28 years were examined using quantitative real-time polymerase chain reaction. Inflammatory markers, such as C-reactive protein (CRP), tumor necrosis factor-alpha (TNF-α), and interleukin (IL)-6, were measured in serum by enzyme immunoassay. ZnT1 and Zip1 were the most abundantly expressed zinc transporters in leukocytes. The mRNA levels of many zinc transporters (ZnT4, ZnT5, ZnT9, Zip1, Zip4, and Zip6) were significantly lower in obese women, and expression of these genes was inversely correlated with BMI and body fat percentage. In addition, inflammatory markers (CRP and TNF-α) were significantly higher in obese women. The mRNA levels of ZnT4, Zip1, and Zip6 were inversely correlated with CRP (P < 0.05), and mRNA levels of ZnT4 and ZnT5 were inversely correlated with TNF-α (P < 0.05). In standardized simple regression models, levels of TNF-α and CRP were negatively associated with mRNA levels of zinc transporters such as ZnT4, ZnT5, Zip1, and Zip6 (P < 0.05). These results suggest that the expression of zinc transporters may be altered in obese individuals. Changes in zinc transporters may also be related to the inflammatory state associated with obesity.

  12. Neurotrophic and inflammatory markers in bipolar disorder: A prospective study.

    PubMed

    van den Ameele, Seline; Coppens, Violette; Schuermans, Jeroen; De Boer, Peter; Timmers, Maarten; Fransen, Erik; Sabbe, Bernard; Morrens, Manuel

    2017-10-01

    Altered neurotrophic signaling is thought to impair neuroplasticity in bipolar disorder (BD). Brain-derived neurotrophic factor (BDNF) is proposed as a neurotrophic marker in BD. However, the current evidence for its use in monitoring disease activity and illness progression is conflicting and an exploration of additional neurotrophic markers is needed. This prospective case-control study investigated mood-specific changes in potential neurotrophic markers and their association to inflammatory activity. Patients with BD were included during an acute mood episode, either depressive (n=35) or (hypo)manic (n=32). Fifty-nine patients (88%) and 29 healthy controls (97%) completed the study. Peripheral blood levels of BDNF, vascular endothelial growth factor A (VEGF), soluble fms-like tyrosine kinase-1 (sFlt-1) and tumor necrosis factor alpha (TNF-α) were measured at baseline and after 2 months. Biomarker levels in patients were compared to controls and correlated to HDRS-17 and YMRS total scores and the PANSS positive subscale scores. Linear mixed model analysis revealed no significant differences in neurotrophic markers between patients and controls. We found significantly increased TNF-α levels in patients and a subsequent normalization during euthymia. None of the biomarkers strongly correlated to mood symptom severity. Despite standardized methodological practices, BDNF and VEGF levels had a wide distribution range. We need a better understanding of methodological aspects influencing the analysis of neurotrophic factors to improve future research on markers for mood state monitoring and illness progression in BD. Copyright © 2017 Elsevier Ltd. All rights reserved.

  13. Effects of periodontal therapy on glycemic control and inflammatory markers.

    PubMed

    O'Connell, Patricia A A; Taba, Mario; Nomizo, Auro; Foss Freitas, Maria C; Suaid, Flavia A; Uyemura, Sergio A; Trevisan, Glauce L; Novaes, Arthur B; Souza, Sergio L S; Palioto, Daniela B; Grisi, Marcio F M

    2008-05-01

    Periodontitis, a complication of diabetes mellitus (DM), can induce or perpetuate systemic conditions. This double-masked, placebo-controlled study evaluated the effects of periodontal therapy (scaling and root planing [SRP]) on the serum levels of glycated hemoglobin (HbA1c) and on inflammatory biomarkers. Thirty subjects with type 2 DM and periodontitis were treated with SRP + placebo (SRP; N = 15) or with SRP + doxycycline (SRP+Doxy; N = 15), 100 mg/day, for 14 days. Clinical and laboratory data were recorded at baseline and at 3 months after treatment. After 3 months, the reduction in probing depth was 0.8 mm for the SRP group (P <0.01) and 1.1 mm for the SRP+Doxy group (P <0.01) followed by a 0.9% (SRP; P = 0.17) and 1.5% (SRP+Doxy; P <0.01) reduction in HbA1c levels. A significant reduction in interleukin (IL)-6; interferon-inducible protein 10; soluble fas ligand; granulocyte colony-stimulating factor; RANTES; and IL-12 p70 serum levels were also verified (N = 30). To our knowledge, this is the first report on the effects of periodontal therapy on multiple systemic inflammatory markers in DM. Periodontal therapy may influence the systemic conditions of patients with type 2 DM, but no statistical difference was observed with the adjunctive systemic doxycycline therapy. Moreover, it is possible that the observed improvement in glycemic control and in the reduction of inflammatory markers could also be due to diet, which was not controlled in our study. Therefore, a confirmatory study with a larger sample size and controlled diet is necessary.

  14. Diagnostic and prognostic significance of inflammatory markers in lung cancer-associated pleural effusions.

    PubMed

    Kotyza, Jaromir; Havel, David; Vrzalová, Jindra; Kulda, Vlastimil; Pesek, Milos

    2010-01-01

    Besides massive expression in inflammatory pleural effusions, inflammatory markers are also present in cancerinduced pleural effusions. Recent advances in cancer biology point to a role of inflammatory signaling in cancer and encourage reconsidering the diagnostic and prognostic value of inflammatory markers. Here an attempt was made to relate protein levels of inflammatory markers to underlying malignant processes in the pleural space. Pleural effusions from lung cancer patients (n=116) were subjected to a multifactorial analysis covering 13 inflammatory markers. The composition of tumor-associated effusions was compared with that of parainflammatory pleural effusions (n=30), transudates (n=18), and serum values, and evaluated in relation to cancer origin, histology, cytology, pleural involvement, treatment history, and survival time. Inflammatory markers were significantly expressed in pleural effusions of paraneoplastic origin when compared to transudates and most serum levels. Values in pleura-invading and metastatic tumor-associated effusions were typically higher than those of other tumors. Many markers correlated negatively with survival, most prominently IL-8 (r=-0.36, p=0.001) and VEGF (r=-0.35, p=0.001). It appears that most inflammatory markers are highly expressed in tumor-associated pleural effusions, reflecting to some extent tumor origin and localization. Despite the lower efficacy of inflammatory markers in the differentiation between exudative pleural effusions, some inflammatory markers may represent potential prognostic markers of malignant processes in the pleural space.

  15. Serum Inflammatory Markers and Preeclampsia in Type 1 Diabetes

    PubMed Central

    Du, Mei; Basu, Arpita; Fu, Dongxu; Wu, Mingyuan; Centola, Michael; Jenkins, Alicia J.; Hanssen, Kristian F.; Garg, Satish K.; Hammad, Samar M.; Scardo, James A.; Aston, Christopher E.; Lyons, Timothy J.

    2013-01-01

    OBJECTIVE Inflammation and endothelial dysfunction have been associated with the immunobiology of preeclampsia (PE), a significant cause of adverse pregnancy outcomes. The prevalence of PE is elevated several fold in the presence of maternal type 1 diabetes mellitus (T1DM). Although cross-sectional studies of pregnancies among women without diabetes have shown altered inflammatory markers in the presence of PE, longitudinal studies of diabetic women are lacking. In maternal serum samples, we examined the temporal associations of markers of inflammation with the subsequent development of PE in women with T1DM. RESEARCH DESIGN AND METHODS We conducted longitudinal analyses of serum C-reactive protein (CRP), adhesion molecules, and cytokines during the first (mean ± SD, 12.2 ± 1.9 weeks), second (21.6 ± 1.5 weeks), and third (31.5 ± 1.7 weeks) trimesters of pregnancy (visits 1–3, respectively). All study visits took place before the onset of PE. Covariates were BMI, HbA1c, age of onset, duration of diabetes, and mean arterial pressure. RESULTS In women with T1DM who developed PE versus those who remained normotensive, CRP tended to be higher at visits 1 (P = 0.07) and 2 (P = 0.06) and was significantly higher at visit 3 (P < 0.05); soluble E-selectin and interferon-γ–inducible protein-10 (IP-10) were significantly higher at visit 3; interleukin-1 receptor antagonist (IL-1ra) and eotaxin were higher and lower, respectively, at visit 2 (all P < 0.05). These conclusions persisted following adjustment for covariates. CONCLUSIONS In pregnant women with T1DM, elevated CRP, soluble E-selectin, IL-1ra, and IP-10 and lower eotaxin were associated with subsequent PE. The role of inflammatory factors as markers and potential mechanisms of the high prevalence of PE in T1DM merits further investigation. PMID:23393212

  16. Inflammatory markers in a randomised soya intervention among men.

    PubMed

    Maskarinec, Gertraud; Oum, Robert; Chaptman, Ann K; Ognjanovic, Simona

    2009-06-01

    The present analysis investigated the effect of soya foods on serum levels of six inflammatory markers, leptin, adiponectin, monocyte attractant protein 1 (MCP-1), macrophage inflammatory protein-1b (MIP-1b), IL-6 and C-reactive protein (CRP), and their relationship with BMI and lifetime soya intake. We randomised twenty-four men to a high- (two daily servings with 30-35 mg isoflavones per serving) or a low-soya diet for 3 months. After a 1-month washout period, the men crossed over to the other treatment. We used a multiplex bead immunoassay to measure leptin, adiponectin, MCP-1 and MIP-1b and ELISA assays for IL-6 and CRP. The statistical analysis applied mixed models that incorporated the four repeated measurements. The men had a mean age of 58.7 (sd 7.2) years and a mean BMI of 28.4 (sd 4.9) kg/m2. We observed no significant intervention effect of the soya treatment on any of the six markers. After adjustment for age and ethnicity, highly significant associations of BMI and body weight with leptin and MCP-1 emerged. Men with high soya intake early in life also had higher levels of leptin and MCP-1, whereas no association was seen for soya intake during adulthood. MIP-1b, adiponectin, IL-6 and CRP were not related to BMI, body weight or soya intake at any time in life. No intervention effect of soya foods on markers of inflammation was observed in this small study, but adiposity and early-life soya intake were related to higher leptin and MCP-1 levels.

  17. Early identification of 'acute-onset' chronic inflammatory demyelinating polyneuropathy.

    PubMed

    Sung, Jia-Ying; Tani, Jowy; Park, Susanna B; Kiernan, Matthew C; Lin, Cindy Shin-Yi

    2014-08-01

    Distinguishing patients with acute-onset chronic inflammatory demyelinating polyneuropathy from acute inflammatory demyelinating polyneuropathy prior to relapse is often challenging at the onset of their clinical presentation. In the present study, nerve excitability tests were used in conjunction with the clinical phenotype and disease staging, to differentiate between patients with acute-onset chronic inflammatory demyelinating polyneuropathy and patients with acute inflammatory demyelinating polyneuropathy at an early stage, with the aim to better guide treatment. Clinical assessment, staging and nerve excitability tests were undertaken on patients initially fulfilling the diagnostic criteria of acute inflammatory demyelinating polyneuropathy soon after symptom onset and their initial presentation. Patients were subsequently followed up for minimum of 12 months to determine if their clinical presentations were more consistent with acute-onset chronic inflammatory demyelinating polyneuropathy. Clinical severity as evaluated by Medical Research Council sum score and Hughes functional grading scale were not significantly different between the two cohorts. There was no difference between the time of onset of initial symptoms and nerve excitability test assessment between the two cohorts nor were there significant differences in conventional nerve conduction study parameters. However, nerve excitability test profiles obtained from patients with acute inflammatory demyelinating polyneuropathy demonstrated abnormalities in the recovery cycle of excitability, including significantly reduced superexcitability (P < 0.001) and prolonged relative refractory period (P < 0.01), without changes in threshold electrotonus. In contrast, in patients with acute-onset chronic inflammatory demyelinating polyneuropathy, a different pattern occurred with the recovery cycle shifted downward (increased superexcitability, P < 0.05; decreased subexcitability, P < 0.05) and increased

  18. Corneal sensitivity in chronic inflammatory demyelinating polyneuropathy.

    PubMed

    Bansal, Surbhi; Myneni, Ajay A; Mu, Lina; Myers, Bennett H; Patel, Sangita P

    2014-07-01

    Neurotrophic keratitis may result from a variety of ocular or systemic diseases. Chronic inflammatory demyelinating polyneuropathy (CIDP) is an autoimmune neuropathy that affects any nerve plexus but with no known association with corneal disease. We observed 2 patients with CIDP and visually compromising neurotrophic corneal ulcers. This study was performed to determine the prevalence of neurotrophic corneas in patients with CIDP to identify a subpopulation of asymptomatic patients who are at risk for vision loss. This is an observational case series of 2 patients with CIDP with visually compromising neurotrophic corneal ulcers and a prospective clinical study comparing corneal sensitivity in 9 patients with CIDP versus 9 age- and sex-matched controls. Corneal sensitivity was tested with an esthesiometer. Statistical analyses were performed to determine patterns or significances in relation to the subject's age, gender, and duration and severity of the disease. The overall median corneal sensitivity was 5.7 for patients with CIDP and 6.0 for controls (P = 0.09). The mean corneal sensitivity was 5.6 ± 0.4 in patients with CIDP compared with 5.8 ± 0.3 in controls. No specific pattern was found with age, gender, or duration and severity of the disease among patients with CIDP. Although the case series demonstrated decreased corneal sensitivity in both patients with CIDP, the prospective study detected reduced corneal sensitivity in patients with CIDP when compared with controls, but did not reach statistical significance. Ophthalmic examinations with measurement of corneal sensitivity should be considered in the management of patients with CIDP.Clinical Trial Registration-URL: http://www.clinicaltrials.gov. Unique identifier: NCT01379833.

  19. Intravenous immunoglobulin for chronic inflammatory demyelinating polyradiculoneuropathy.

    PubMed

    Van Schaik, I N; Winer, J B; De Haan, R; Vermeulen, M

    2002-01-01

    Chronic inflammatory demyelinating polyradiculoneuropathy is an immune mediated disorder characterised by progressive or relapsing symmetrical motor or sensory symptoms and signs in more than one limb, developing over at least two months. It may cause prolonged periods of disability and even death. Several uncontrolled studies have suggested a beneficial effect of intravenous immunoglobulin. To review systematically the evidence from randomised controlled trials concerning the efficacy and safety of intravenous immunoglobulin in chronic inflammatory demyelinating polyradiculoneuropathy. We used the Search Strategy of the Cochrane Neuromuscular Disease Review Group to search the Disease Group register and other databases for randomised controlled trials from 1985 onwards. Randomised controlled studies examining the effects of any dose of intravenous immunoglobulin versus placebo, plasma exchange or corticosteroids in patients with definite or probable chronic inflammatory demyelinating polyradiculoneuropathy. Outcome measures had to include one of the following: a disability score, the Medical Research Council sum score, electrophysiological data or walking distance. Studies which reported the frequency of adverse effects were used to assess the safety of treatment. Two reviewers independently reviewed literature searches to identify potentially relevant trials, scored their quality and extracted data independently. For dichotomous data, we calculated relative risks, and for continuous data, effect sizes (for definition see statistical analysis section) and weighted pooled effect sizes. Statistical uncertainty was expressed in 95% confidence intervals. Sensitivity analysis excluding studies with quality scores below A 0.50 and below B 0.75 was planned but not performed as all studies had quality scores above 0.75. Six randomised controlled trials were considered eligible including 170 patients. Four studies on 113 patients compared intravenous immunoglobulin against

  20. Association between dietary inflammatory index and inflammatory markers in the HELENA study.

    PubMed

    Shivappa, Nitin; Hebert, James R; Marcos, Ascensión; Diaz, Ligia-Esperanza; Gomez, Sonia; Nova, Esther; Michels, Nathalie; Arouca, Aline; González-Gil, Esther; Frederic, Gottrand; González-Gross, Marcela; Castillo, Manuel J; Manios, Yannis; Kersting, Mathilde; Gunter, Marc J; De Henauw, Stefaan; Antonios, Kafatos; Widhalm, Kurt; Molnar, Denes; Moreno, Luis; Huybrechts, Inge

    2017-06-01

    Previous research has shown that diet is associated with low-grade systemic inflammation among adults. However, no study has yet been conducted to explore the association between inflammatory potential of diet and low-grade systemic inflammation among adolescents whose dietary behavior may be different from adults. We examine the predictive ability of 24-h recall-derived dietary inflammatory index (DII) scores on inflammation among 532 European adolescents in the HELENA cross-sectional study. The DII is a literature-derived dietary index developed to predict inflammation. The DII was calculated per 1000 calories and was tested against C-reactive protein, ILs-1,2,4,10, TNF-α, ICAM, vascular cell adhesion molecule (VCAM), and IFN-γ. All inflammatory markers had nonnormal distributions and therefore were log transformed. Analyses were performed using multivariable linear regression, adjusting for age, sex, city, BMI, smoking, and physical activity. Pro-inflammatory diet (higher DII scores) was associated with increased levels of various inflammatory markers: TNF-α, IL-1, 2, IFN-γ,  and vascular cell adhesion molecule (bDIIt3vs1 = 0.13, 95% CI: 0.001, 0.25; 0.13, 95% CI 0.001, 0.25; 0.40, 95% CI: 0.03, 0.77; 0.53, 95% CI: 0.05, 1.01; 0.07, 95% CI: 0.01, 0.13, respectively). These results reinforce the fact that diet, as a whole, plays an important role in modifying inflammation in adolescents. © 2016 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

  1. Chronic Inflammatory Disease, Lifestyle and Treatment Response

    ClinicalTrials.gov

    2017-05-30

    Autoimmune Diseases; Inflammatory Bowel Diseases; Crohn Disease (CD); Colitis, Ulcerative (UC); Arthritis, Rheumatoid (RA); Spondylarthropathies; Arthritis, Psoriatic (PsA); Psoriasis; Hidradenitis Suppurativa (HS); Uveitis

  2. Inflammatory markers and exposure to occupational air pollutants.

    PubMed

    Ohlson, Carl-Göran; Berg, Peter; Bryngelsson, Ing-Liss; Elihn, Karine; Ngo, Yen; Westberg, Håkan; Sjögren, Bengt

    2010-11-01

    To study the possible relationship between inhalation of airborne particles in the work environment and inflammatory markers in blood. Total dust was sampled in the breathing zone of 73 subjects working with welding, cutting, grinding and in foundries such as iron, aluminium, and concrete. Stationary measurements were used to study different size fractions of particles including respirable dust, particulate matter (PM)(10) and PM(2.5), the particle number concentration, the number of particles deposited in the alveoli, and total particle surface area concentration. Inflammatory markers such as interleukin-6 (IL-6), C-reactive protein (CRP), fibrinogen, d-dimer, and urate were measured in plasma or serum before the first shift after the summer vacation and after the first, second, and fourth shift. The mean level of total dust in the breathing zone was 0.93 mg/m(3). The proxies for mean respirable dust fraction was 0.27 mg/m(3), PM(10) 0.60 mg/m(3), and PM(2.5) was 0.31 mg/m(3). The IL-6 values increased by 50% after the first day, but decreased after shift on the second and fourth day. CRP did not increase after the first shift but increased by 17% after the second shift. Other biomarkers were unaffected. A multiple linear regression analysis of a subgroup of 47 subjects showed a statistically significant positive relationship between particle exposure and post-shift IL-6. This study supports previous investigations observing increases of IL-6 at air concentrations of PM(10) or PM(2.5) between 0.13 and 0.3 mg/m(3) among healthy subjects. This increase of IL-6 may indicate an increased risk of coronary heart disease.

  3. Intravenous immunoglobulin for chronic inflammatory demyelinating polyradiculoneuropathy.

    PubMed

    Eftimov, Filip; Winer, John B; Vermeulen, Marinus; de Haan, Rob; van Schaik, Ivo N

    2009-01-21

    Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) causes progressive or relapsing weakness and numbness of the limbs, developing over at least two months. Uncontrolled studies suggest that intravenous immunoglobulin (IVIg) helps. To review systematically the evidence from randomised controlled trials concerning the efficacy and safety of IVIg in CIDP. We searched the Cochrane Neuromuscular Trials Register, MEDLINE, EMBASE and ISI from January 1985 to May 2008. Randomised controlled studies testing any dose of IVIg versus placebo, plasma exchange or corticosteroids in definite or probable CIDP. Two authors reviewed literature searches to identify potentially relevant trials, scored their quality and extracted data independently. We contacted authors for additional information. Seven randomised controlled trials were considered eligible including 287 participants. These trials were homogeneous and overall quality was high. Five studies on 235 participants compared IVIg against placebo. One trial with 20 participants compared IVIg with plasma exchange and one trial compared IVIg with prednisolone in 32 participants. A significantly higher proportion of participants improved in disability within one month after IVIg treatment as compared with placebo (relative risk 2.40, 95% confidence interval 1.72 to 3.36). Whether all these improvements are equally clinically relevant cannot be deduced from this analysis because each trial used different disability scales and definitions of significant improvement. In three trials including 84 participants the disability could be transformed to the modified Rankin score, on which significantly more patients improved one point after IVIg treatment compared to placebo (relative risk 2.40, 95% confidence interval 0.98 to 5.83). Only one study included in this review had a long-term follow-up. The results of this study suggest that intravenous immunoglobulin improves disability more than placebo over 24 and 48 weeks. The

  4. Sleep deprivation affects inflammatory marker expression in adipose tissue

    PubMed Central

    2010-01-01

    Sleep deprivation has been shown to increase inflammatory markers in rat sera and peripheral blood mononuclear cells. Inflammation is a condition associated with pathologies such as obesity, cancer, and cardiovascular diseases. We investigated changes in the pro and anti-inflammatory cytokines and adipokines in different depots of white adipose tissue in rats. We also assessed lipid profiles and serum levels of corticosterone, leptin, and adiponectin after 96 hours of sleep deprivation. Methods The study consisted of two groups: a control (C) group and a paradoxical sleep deprivation by 96 h (PSD) group. Ten rats were randomly assigned to either the control group (C) or the PSD. Mesenteric (MEAT) and retroperitoneal (RPAT) adipose tissue, liver and serum were collected following completion of the PSD protocol. Levels of interleukin (IL)-6, interleukin (IL)-10 and tumour necrosis factor (TNF)-α were analysed in MEAT and RPAT, and leptin, adiponectin, glucose, corticosterone and lipid profile levels were analysed in serum. Results IL-6 levels were elevated in RPAT but remained unchanged in MEAT after PSD. IL-10 protein concentration was not altered in either depot, and TNF-α levels decreased in MEAT. Glucose, triglycerides (TG), VLDL and leptin decreased in serum after 96 hours of PSD; adiponectin was not altered and corticosterone was increased. Conclusion PSD decreased fat mass and may modulate the cytokine content in different depots of adipose tissue. The inflammatory response was diminished in both depots of adipose tissue, with increased IL-6 levels in RPAT and decreased TNF-α protein concentrations in MEAT and increased levels of corticosterone in serum. PMID:21034496

  5. Mould exposure at home relates to inflammatory markers in blood.

    PubMed

    Beijer, L; Thorn, J; Rylander, R

    2003-02-01

    Living in damp buildings has been associated with airway symptoms, suspected to be due to inflammatory reactions. The relationship between home exposure to mould and signs of inflammation was, therefore, studied. Nonsmoking subjects with a high (G-high, > 4.0 ng x m(-3), n = 17) or low (G-low, < 2.0 ng x m(-3), n = 18) amount of airborne beta(1 --> 3)-D-glucan, an indicator of mould biomass, in the home were recruited. Blood samples were analysed for granulocytic enzymes, T-cell subsets and the secretion of cytokines from in vitro incubated peripheral blood mononuclear cells (PBMCs). In the G-high group, the proportion of cytotoxic T-cells (CD8+S6F1+) was lower and secretion of tumour necrosis factor-alpha from PBMCs higher than in the G-low group. There were no significant differences in secretion of interferon gamma and interleukin (IL)-4 from PBMCs between the two groups. Among nonatopic subjects, the ratio between interferon gamma and IL-4 was significantly higher in the G-high group than in the G-low group and was related to the amount of beta(1 --> 3)-D-glucan in the home. No significant differences were found regarding secretion of IL-10 or IL-Ibeta from PBMCs, eosinophil cationic protein or myeloperoxidase in serum, or differential cell counts in blood. The effects found on inflammatory markers in relation to beta(1 --> 3)-D-glucan in the home suggest upregulation of some parts of the inflammatory/immunological system due to mould exposure.

  6. Enhanced Gamma Oscillatory Activity in Rats with Chronic Inflammatory Pain

    PubMed Central

    Wang, Jing; Wang, Jing; Xing, Guo-Gang; Li, Xiaoli; Wan, You

    2016-01-01

    It has been reported that oscillatory gamma activity participates in brief acute pain and tonic ongoing pain. It is of great interest to determine whether the gamma activity is involved in chronic pain since chronic pain is a more severe pathological condition characterized by pain persistency. To investigate the oscillatory gamma activity in chronic pain, in the present study, we recorded spontaneous electrocorticogram (ECoG) signals during chronic pain development in rats with chronic inflammatory pain induced by monoarthritis. Power spectrum analysis of ECoG data showed that gamma power increased significantly at the late stage of chronic inflammatory pain. The increased gamma activity occurred mainly at electrodes over primary somatosensory cortices. In rats with chronic pain, the gamma power was positively correlated with the hyperalgesia measured by laser energy that elicited hindpaw withdrawal response. Furthermore, an increased coupling between the amplitude of gamma power and the phase of theta oscillations was observed in chronic inflammatory pain condition. These results indicate an enhanced spontaneous gamma activity in chronic pain and suggest a potential biomarker for the severity of chronic pain. PMID:27847461

  7. Arresting the Inflammatory Drive of Chronic Lymphocytic Leukemia with Ibrutinib

    PubMed Central

    Bachireddy, Pavan; Wu, Catherine J.

    2016-01-01

    Summary The clinical success of agents targeting the B cell receptor (BCR) signaling pathway in chronic lymphocytic leukemia (CLL) may also derive from disrupting the CLL microenvironment. Investigation of the immunomodulatory effects of these agents illuminates the unique immunobiology of CLL and highlights potential targets for dismantling the chronic inflammatory drive. PMID:26847060

  8. Motor variant of chronic inflammatory demyelinating polyneuropathy in a child.

    PubMed

    Sinno, Durriyah D; Darras, Basil T; Yamout, Bassem I; Rebeiz, Jean G; Mikati, Mohamad A

    2008-06-01

    Only 2 cases of pure motor chronic demyelinating inflammatory polyneuropathy in the pediatric age group have been reported in the literature. We report on a motor variant of chronic demyelinating inflammatory polyneuropathy with anti-ganglioside antibodies, diagnosed in a 5-year-old girl who presented with progressive motor weakness over a period of 12 months with no sensory involvement. She initially responded partially to intravenous immunoglobulin therapy (1 gm/kg/month for 6 months), and then demonstrated sustained but incomplete improvement on chronic prednisone therapy (1-2 mg/kg/day), on which she has continued since 1 year and 4 months after her initial presentation 3 years ago.

  9. New anti-inflammatory targets for chronic obstructive pulmonary disease.

    PubMed

    Barnes, Peter J

    2013-07-01

    Chronic obstructive pulmonary disease (COPD) is associated with chronic inflammation of the peripheral airways and lung parenchyma, which leads to progressive obstruction of the airways. Current management with long-acting bronchodilators does not reduce disease progression, and there are no treatments that effectively suppress chronic inflammation in COPD. An increased understanding of the inflammatory processes that are involved in the pathophysiology of COPD has identified several new therapeutic targets. This Review discusses some of the most promising of these targets, including new antioxidants, kinase inhibitors and drugs that target cellular senescence, microbial colonization, epigenetic regulation of inflammatory gene expression and corticosteroid resistance.

  10. Acute clinical onset chronic inflammatory demyelinating polyneuropathy in a dog.

    PubMed

    Molín, Jéssica; Márquez, Mercedes; Raurell, Xavier; Matiasek, Kaspar; Ferrer, Isidre; Pumarola, Martí

    2011-09-01

    We report a case of acute-onset ambulatory paraparesis with electrophysiological abnormalities compatible with axonal and demyelinating lesions in a Rottweiler dog. Although the clinical findings were compatible with acute canine idiopathic polyneuropathy, postmortem investigations revealed a chronic demyelinating polyneuropathy affecting the nerve roots. Due to the combination of acute clinical presentation and chronic pathologic features, this case is consistent with the acute-onset form of chronic inflammatory demyelinating polyneuropathy (A-CIDP).

  11. Inflammatory bowel diseases, chronic liver diseases and the lung.

    PubMed

    Rodriguez-Roisin, Roberto; Bartolome, Sonja D; Huchon, Gérard; Krowka, Michael J

    2016-02-01

    This review is devoted to the distinct associations of inflammatory bowel diseases (IBD) and chronic liver disorders with chronic airway diseases, namely chronic obstructive pulmonary disease and bronchial asthma, and other chronic respiratory disorders in the adult population. While there is strong evidence for the association of chronic airway diseases with IBD, the data are much weaker for the interplay between lung and liver multimorbidities. The association of IBD, encompassing Crohn's disease and ulcerative colitis, with pulmonary disorders is underlined by their heterogeneous respiratory manifestations and impact on chronic airway diseases. The potential relationship between the two most prevalent liver-induced pulmonary vascular entities, i.e. portopulmonary hypertension and hepatopulmonary syndrome, and also between liver disease and other chronic respiratory diseases is also approached. Abnormal lung function tests in liver diseases are described and the role of increased serum bilirubin levels on chronic respiratory problems are considered. Copyright ©ERS 2016.

  12. Intravenous immunoglobulin for chronic inflammatory demyelinating polyradiculoneuropathy.

    PubMed

    Eftimov, Filip; Winer, John B; Vermeulen, Marinus; de Haan, Rob; van Schaik, Ivo N

    2013-12-30

    Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) causes progressive or relapsing weakness and numbness of the limbs, developing over at least two months. Uncontrolled studies suggest that intravenous immunoglobulin (IVIg) helps. This review was first published in 2002 and has since been updated, most recently in 2013. To review systematically the evidence from randomised controlled trials (RCTs) concerning the efficacy and safety of IVIg in CIDP. On 4 December 2012, we searched the Cochrane Neuromuscular Disease Group Specialized Register, CENTRAL (2012, issue 11 in the Cochrane Library), MEDLINE and EMBASE to December 2012 and ISI from January 1985 to May 2008. We searched for ongoing trials through two metaRegistries (World Health Organization International Clinical Trials Registry Platform Search Portal and Current Controlled Trials). We selected RCTs testing any dose of IVIg versus placebo, plasma exchange or corticosteroids in definite or probable CIDP. Two authors reviewed literature searches to identify potentially relevant RCTs, scored their quality and extracted data independently. We contacted authors for additional information. We considered eight RCTs, including 332 participants, to be eligible for inclusion in the review. These trials were homogeneous and the overall risk of bias low. Five studies, in a total of 235 participants compared IVIg against placebo. One trial with 20 participants compared IVIg with plasma exchange, one trial compared IVIg with prednisolone in 32 participants, and one trial, newly included at this update, compared IVIg with intravenous methylprednisolone in 46 participants.A significantly higher proportion of participants improved in disability within one month after IVIg treatment as compared with placebo (risk ratio (RR) 2.40, 95% confidence interval (CI) 1.72 to 3.36; number needed to treat for an additional beneficial outcome 3.03 (95% CI 2.33 to 4.55), high quality evidence). Whether all these improvements

  13. [Persistence of chronic inflammatory responses, role in the development of chronic pancreatitis, obesity and pancreatic cancer].

    PubMed

    Khristich, T N

    2014-11-01

    The purpose of the review--to analyze the basic data of the role of chronic low-intensity inflammatory response as general biological process in the development and progression of chronic pancreatitis, obesity, and pancreatic cancer. Highlighted evidence from epidemiological studies showing that chronic pancreatitis and obesity are independent risk factors for pancreatic cancer, regardless of diabetes. Studied role of adipokines as Cytokines regulating of immune inflammatory response. Draws attention to the staging of pancreatic cancer in obesity.

  14. The effect of smoking on inflammatory and bone remodeling markers in gingival crevicular fluid and subgingival microbiota following periodontal therapy.

    PubMed

    Bunaes, D F; Mustafa, M; Mohamed, H G; Lie, S A; Leknes, K N

    2017-08-01

    Periodontal health is mediated by suppressing microorganisms inducing a local inflammatory host response. Smoking may impair this process. This study compares gingival crevicular fluid levels of inflammatory and bone remodeling markers in heavy smokers and non-smokers following active and supportive periodontal therapy in patients with chronic periodontitis. Gingival crevicular fluid and subgingival plaque were collected from the deepest periodontal pocket in 50 patients, 25 smokers and 25 non-smokers, at baseline (T0), following active (T1) and 12 mo of supportive periodontal therapy (T2). Smoking status was validated measuring serum cotinine levels. Gingival crevicular fluid levels of 27 inflammatory and two bone remodeling markers were analyzed using multiplex and singleplex micro-bed immunoassays, and subgingival plaque samples using checkerboard DNA-DNA hybridization. Amounts of markers in smokers and non-smokers were compared calculating the effect size. Expression of inflammatory and bone-remodeling markers in smokers demonstrated an overall reduced effect size at T0 and T2 (p < 0.001). In particular, proinflammatory markers (p < 0.001), chemokines (p = 0.007) and growth factors (p = 0.003) at T0, osteoprotegerin (p = 0.003) at T1, proinflammatory markers (p = 0.019) and chemokines (p = 0.005) at T2. At T2, interleukin-8 was detected in significantly higher levels in smokers. Ten different markers in non-smokers and none in smokers responded to periodontal therapy (p < 0.05). An overall negative association was revealed between smoking and subgroups of markers at sites presenting ≥ 10(5) red complex periodontal microbial species. Except for an upregulation of interleukin-8, smokers exhibited reduced gingival crevicular fluid levels of several inflammatory markers at baseline and following active and supportive periodontal therapy. Only inflammatory responses in non-smokers adapted to periodontal therapy. Apparently, there seems to be an immunosuppressant

  15. Circulating Adipokines and Inflammatory Markers and Postmenopausal Breast Cancer Risk

    PubMed Central

    Wang, Tao; Cushman, Mary; Xue, Xiaonan; Wassertheil-Smoller, Sylvia; Strickler, Howard D.; Rohan, Thomas E.; Manson, JoAnn E.; McTiernan, Anne; Kaplan, Robert C.; Scherer, Philipp E.; Chlebowski, Rowan T.; Snetselaar, Linda; Wang, Dan; Ho, Gloria Y. F.

    2015-01-01

    Background: Adipokines and inflammation may provide a mechanistic link between obesity and postmenopausal breast cancer, yet epidemiologic data on their associations with breast cancer risk are limited. Methods: In a case-cohort analysis nested within the Women’s Health Initiative Observational Study, a prospective cohort of postmenopausal women, baseline plasma samples from 875 incident breast cancer case patients and 839 subcohort participants were tested for levels of seven adipokines, namely leptin, adiponectin, resistin, interleukin-6, tumor necrosis factor-α, hepatocyte growth factor, and plasminogen activator inhibitor-1, and for C-reactive protein (CRP), an inflammatory marker. Data were analyzed by multivariable Cox modeling that included established breast cancer risk factors and previously measured estradiol and insulin levels. All statistical tests were two-sided. Results: The association between plasma CRP levels and breast cancer risk was dependent on hormone therapy (HT) use at baseline (P interaction = .003). In a model that controlled for multiple breast cancer risk factors including body mass index (BMI), estradiol, and insulin, CRP level was positively associated with breast cancer risk among HT nonusers (hazard ratio for high vs low CRP levels = 1.67, 95% confidence interval = 1.04 to 2.68, P trend = .029). None of the other adipokines were statistically significantly associated with breast cancer risk. Following inclusion of CRP, insulin, and estradiol in a multivariable model, the association of BMI with breast cancer was attenuated by 115%. Conclusion: These data indicate that CRP is a risk factor for postmenopausal breast cancer among HT nonusers. Inflammatory mediators, together with insulin and estrogen, may play a role in the obesity–breast cancer relation. PMID:26185195

  16. The inflammatory markers in polycystic ovary syndrome: association with obesity and IVF outcomes.

    PubMed

    Çakıroğlu, Y; Vural, F; Vural, B

    2016-08-01

    To investigate the inflammatory markers in polycystic ovary syndrome (PCOS) and associations of these markers with obesity and in vitro fertilization (IVF) outcomes. A total of 292 women underwent IVF procedure either with PCOS (n = 146) or without PCOS (n = 146, age, and body mass index (BMI) matched controls) were included in the study. All patients were classified according to BMI levels (normal weight: NW, BMI <25 kg/m(2) and obese: OB, BMI ≥25 kg/m(2)). The inflammatory markers were leukocyte count, neutrophil/lymphocyte ratio (NLR), platelet/lymphocyte ratio (PLR), mean platelet volume (MPV). BMI of PCOS was positively correlated with leukocyte, neutrophil, lymphocyte and MPV (p < 0.05), but negatively correlated with NLR and PLR (p < 0.05). Both NLR and PLR increased significantly in PCOS (p < 0.001). PLR increased significantly in NW-PCOS compared the NW-controls and OB-PCOS. MPV values increased only in OB-PCOS subjects. The logistic regression analyzes showed that MPV was the independent variable in PCOS to effect CPR (p = 0.000; OR 0.1; CI 0.06-0.2). NLR and PLR were significantly increased in all PCOS subjects compared to the BMI-matched controls. Despite PLR being decreased by adiposity, PLR increased in NW-PCOS. These results are supporting the hypothesis that PCOS is a chronic inflammatory process independent of obesity. MPV levels were independently associated with CPR in PCOS. Further prospective studies concerning inflammation and IVF outcomes of PCOS are needed.

  17. Antagonistic characteristics are positively associated with inflammatory markers independently of trait negative emotionality.

    PubMed

    Marsland, Anna L; Prather, Aric A; Petersen, Karen L; Cohen, Sheldon; Manuck, Stephen B

    2008-07-01

    Recent evidence suggests that individuals with certain personality traits are at elevated risk for chronic systemic inflammation. To date, this literature has focused on the related traits of hostility and negative affect (NA). In this study, we examine the covariation of trait measures of hostility and NA with the inflammatory mediators interleukin-6 and C-reactive protein. We also explore whether observed associations reflect independent contributions of cognitive, affective and behavioral components of hostile dispositions or shared trait variance with global negative affectivity. Subjects were a diverse sample of 855 relatively healthy middle-aged community volunteers (50% male) from the Adult Health and Behavior Project. The Buss and Perry Aggression Questionnaire (BPAQ) and an Abbreviated Cook-Medley Hostility Scale (ACM) were used to measure dimensions of hostility, and the Multidimensional Personality Questionnaire was used to measure trait NA. Regression analyses accounting for demographic characteristics and medical covariates showed a positive relationship of all components of hostility and trait NA with both IL-6 and CRP. After controlling for trait NA, only the behavioral component of hostility was independently associated with the inflammatory markers. The relationships of cognitive and affective components of hostility with inflammatory markers were largely explained by lifestyle factors, particularly body mass index and smoking. In contrast, lifestyle factors did not explain the covariation of hostile behavioral tendencies and inflammation. These findings suggest that unique attributes of aggressive behavioral tendencies account for much of the variability in inflammation associated with hostility and negative emotions, raising the possibility that individuals high in aggression are at increased risk of inflammatory disease.

  18. Proteomics and chronic inflammatory bowel diseases.

    PubMed

    Felley-Bosco, Emanuela; André, Muriel

    2004-01-01

    Inflammatory bowel diseases (IBD) are relatively frequent in developed countries. Physiopathological events involved in the etiology of IBDs include activation of immune, mesenchymal and epithelial cells. This review gives an overview of the currently applied proteomics technologies. It describes metabolic changes and goes into the approaches using this methodology to understand the molecular mechanisms implicated in the development of the disease.

  19. [Chronic inflammatory bowel diseases and nutrition].

    PubMed

    Meier, R

    1996-01-01

    The etiology of inflammatory bowel disease is still unknown. Several potential mechanisms are discussed. The etiological and therapeutic importance of nutrition is controversial. Though changes in dietary habits and incidence of inflammatory bowel disease during the last century were in parallel, no specific nutritional factor has been isolated. No dietary prophylaxis of inflammatory bowel disease is yet known; all dietary therapies in inflammatory bowel disease aim to improve nutritional support and to diminish inflammation by bowel rest. Children and adolescents gain in weight and height. Total parenteral nutrition will not substantially reduce disease activity and operation rates. Total parenteral nutrition can only be recommended in ulcerative colitis patients with severe disease in the initial phase and in Crohn's patients with severe malnutrition and intestinal complications. Enteral nutrition support is less effective in ulcerative colitis than in Crohn's disease. Reported remission rates on enteral nutrition are 25% for ulcerative colitis and up to 80% for Crohn. However, in active Crohn's disease enteral nutrition is less effective than standard therapy with methylprednisolone and sulfasalizine. It is generally believed that nutrition therapy in combination with drugs is the best treatment modality. There is no evidence to support the importance of any combination of the formula diets such as elemental, oligopeptide, or polymeric formulations. Administration of formula diets by nasogastric tubes all show similar remission rates. Whether newer diets supplemented with arginine, glutamine, omega-3-fatty acids or short chain fatty acids increase remission rates is not known. Further studies in this field are warranted.

  20. Peripheral Inflammatory Markers Contributing to Comorbidities in Autism.

    PubMed

    Inga Jácome, Martha Cecilia; Morales Chacòn, Lilia Maria; Vera Cuesta, Hector; Maragoto Rizo, Carlos; Whilby Santiesteban, Mabel; Ramos Hernandez, Lesyanis; Noris García, Elena; González Fraguela, Maria Elena; Fernandez Verdecia, Caridad Ivette; Vegas Hurtado, Yamilé; Siniscalco, Dario; Gonçalves, Carlos Alberto; Robinson-Agramonte, Maria de Los Angeles

    2016-12-14

    This study evaluates the contribution of peripheral biomarkers to comorbidities and clinical findings in autism. Seventeen autistic children and age-matched typically developing (AMTD), between three to nine years old were evaluated. The diagnostic followed the Diagnostic and Statistical Manual of Mental Disorders 4th Edition (DMS-IV) and the Childhood Autism Rating Scale (CARS) was applied to classify the severity. Cytokine profile was evaluated in plasma using a sandwich type ELISA. Paraclinical events included electroencephalography (EEG) record. Statistical analysis was done to explore significant differences in cytokine profile between autism and AMTD groups and respect clinical and paraclinical parameters. Significant differences were found to IL-1β, IL-6, IL-17, IL-12p40, and IL-12p70 cytokines in individuals with autism compared with AMTD (p < 0.05). All autistic patients showed interictalepileptiform activity at EEG, however, only 37.5% suffered epilepsy. There was not a regional focalization of the abnormalities that were detectable with EEG in autistic patients with history of epilepsy. A higher IL-6 level was observed in patients without history of epilepsy with interictalepileptiform activity in the frontal brain region, p < 0.05. In conclusion, peripheral inflammatory markers might be useful as potential biomarkers to predict comorbidities in autism as well as reinforce and aid informed decision-making related to EEG findings in children with Autism spectrum disorders (ASD).

  1. Frailty and inflammatory markers in older adults with cancer.

    PubMed

    Nishijima, Tomohiro F; Deal, Allison M; Williams, Grant R; Guerard, Emily J; Nyrop, Kirsten A; Muss, Hyman B

    2017-03-08

    We examined the associations between frailty and inflammatory markers, in particular neutrophil lymphocyte ratio (NLR), in elderly cancer patients. We conducted cross-sectional analyses of data derived from the Carolina Seniors Registry (CSR), a database of geriatric assessments (GA) in older adults (≧65 years) with cancer. We included patients in the CSR who had a GA and complete blood count test before initiation of therapy. The primary outcome was frailty, determined using the 36-item Carolina Frailty Index (CFI). In our sample of 133 patients, the median age was 74, and 54% were robust, 22% were pre-frail, and 24% were frail. There was a significant positive correlation between CFI and NLR (r = 0.22, p = 0.025). In multivariable analysis, patients in the top tertile of NLR had an odds ratio of 3.8 (95% CI = 1.1-12.8) for frail/pre-frail status, adjusting for age, sex, race, education level, marital status, cancer type and stage. In bivariable analyses, higher NLR was associated with lower instrumental activity of daily living (IADL) score (p = 0.040) and prolonged timed up and go (p = 0.016). This study suggests an association between frailty and inflammation in older adults with cancer.

  2. Peripheral Inflammatory Markers Contributing to Comorbidities in Autism

    PubMed Central

    Inga Jácome, Martha Cecilia; Morales Chacòn, Lilia Maria; Vera Cuesta, Hector; Maragoto Rizo, Carlos; Whilby Santiesteban, Mabel; Ramos Hernandez, Lesyanis; Noris García, Elena; González Fraguela, Maria Elena; Fernandez Verdecia, Caridad Ivette; Vegas Hurtado, Yamilé; Siniscalco, Dario; Gonçalves, Carlos Alberto; Robinson-Agramonte, Maria de los Angeles

    2016-01-01

    This study evaluates the contribution of peripheral biomarkers to comorbidities and clinical findings in autism. Seventeen autistic children and age-matched typically developing (AMTD), between three to nine years old were evaluated. The diagnostic followed the Diagnostic and Statistical Manual of Mental Disorders 4th Edition (DMS-IV) and the Childhood Autism Rating Scale (CARS) was applied to classify the severity. Cytokine profile was evaluated in plasma using a sandwich type ELISA. Paraclinical events included electroencephalography (EEG) record. Statistical analysis was done to explore significant differences in cytokine profile between autism and AMTD groups and respect clinical and paraclinical parameters. Significant differences were found to IL-1β, IL-6, IL-17, IL-12p40, and IL-12p70 cytokines in individuals with autism compared with AMTD (p < 0.05). All autistic patients showed interictalepileptiform activity at EEG, however, only 37.5% suffered epilepsy. There was not a regional focalization of the abnormalities that were detectable with EEG in autistic patients with history of epilepsy. A higher IL-6 level was observed in patients without history of epilepsy with interictalepileptiform activity in the frontal brain region, p < 0.05. In conclusion, peripheral inflammatory markers might be useful as potential biomarkers to predict comorbidities in autism as well as reinforce and aid informed decision-making related to EEG findings in children with Autism spectrum disorders (ASD). PMID:27983615

  3. Chronic inflammatory demyelinating polyneuropathy in common variable immunodeficiency.

    PubMed

    Özdemir, Özlem; Okan, Mehmet S; Kilic, Sara S

    2012-04-01

    Common variable immunodeficiency comprises a heterogeneous group of primary antibody deficiencies with complex clinical and immunologic phenotypes. Immune dysregulation leads to the generation of multiple autoantibodies against various antigenic targets in patients with common variable immunodeficiency. Chronic inflammatory demyelinating polyneuropathy is a heterogeneous disorder that indicates an autoimmune response against peripheral nerve myelin. We describe a 7-year-old girl with common variable immunodeficiency who developed chronic inflammatory polyneuropathy. A 5-day course of intravenous immunoglobulin (500 mg/kg/day) improved her neurologic disorder. Chronic inflammatory demyelinating polyneuropathy should be added to the broadening spectrum of neurologic complications in common variable immunodeficiency. Early detection and consequent treatment may reverse the neurologic sequelae.

  4. Relationships of inflammatory and haemostatic markers with social class: results from a population-based study of older men.

    PubMed

    Ramsay, Sheena; Lowe, Gordon D O; Whincup, Peter H; Rumley, Ann; Morris, Richard W; Wannamethee, S Goya

    2008-04-01

    Haemostatic and inflammatory markers have been hypothesised to mediate the relationship of social class and cardiovascular disease (CVD). We investigated whether a range of inflammatory/haemostatic markers are associated with social class independent of chronic diseases and behavioural risk factors in a population-based sample of 2682 British men aged 60-79 without a physician diagnosis of CVD, diabetes or musculoskeletal disease requiring anti-inflammatory medications. Men in lower social classes had higher mean levels of C-reactive protein, fibrinogen, interleukin-6, white blood cell count, von Willebrand factor (vWF), factor VIII, activated protein C (APC) resistance, plasma viscosity, fibrin D-dimer and platelet count, compared to higher social class groups; but not of tissue plasminogen activator antigen, haematocrit or activated partial prothrombin time. After adjustment for behavioural risk factors (smoking, alcohol, physical activity and body mass), the associations of social class with vWF, factor VIII, APC resistance, plasma viscosity, and platelet count though weakened, remained statistically significant, while those of other markers were considerably attenuated. In this study of older men without CVD, the social gradient in inflammatory and haemostatic markers was substantially explained by behavioural risk factors. The effect of socio-economic gradient on the factor VIII-vWF complex, APC resistance, plasma viscosity and platelet count merits further study.

  5. Macrolides in Chronic Inflammatory Skin Disorders

    PubMed Central

    Alzolibani, Abdullateef A.; Zedan, Khaled

    2012-01-01

    Long-term therapy with the macrolide antibiotic erythromycin was shown to alter the clinical course of diffuse panbronchiolitis in the late 1980s. Since that time, macrolides have been found to have a large number of anti-inflammatory properties in addition to being antimicrobials. These observations provided the rationale for many studies performed to assess the usefulness of macrolides in other inflammatory diseases including skin and hair disorders, such as rosacea, psoriasis, pityriasis rosea, alopecia areata, bullous pemphigoid, and pityriasis lichenoides. This paper summarizes a collection of clinical studies and case reports dealing with the potential benefits of macrolides antibiotics in the treatment of selected dermatoses which have primarily been classified as noninfectious and demonstrating their potential for being disease-modifying agents. PMID:22685371

  6. Association between a Healthy Lifestyle Score and inflammatory markers among Puerto Rican adults.

    PubMed

    Sotos-Prieto, M; Bhupathiraju, S N; Falcon, L M; Gao, X; Tucker, K L; Mattei, J

    2016-03-01

    The relationship between multiple lifestyle components analyzed in combination and inflammation remains understudied. We aimed to assess the association between a Healthy Lifestyle Score (HLS) that includes adherence to five behavioral components (diet, physical activity and sedentary behaviors, smoking, social support and network, and sleep) and inflammatory markers, as well as the role of the HLS in inflammation among individuals with cardiometabolic conditions, in Puerto Rican adults. In a cross-sectional study of 842 Puerto Ricans adults (aged 45-75 y) living in Boston, MA, the HLS (range = 0-190; maximum indicative of healthiest adherence) was analyzed for association with three inflammatory markers: interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and C-reactive protein (CRP). In multivariable-adjusted models, the HLS was inversely associated with IL-6 (β ± SE = -0.55 ± 0.13; P < 0.001) and TNF-α (-0.39 ± 0.13; P = 0.004). The dietary and smoking components were associated with both inflammatory markers independently of the other HLS components. Significant inverse associations were observed for each 20-unit increase in HLS and IL-6 and TNF-α for participants with hypertension (n = 600; β ± SE = -0.58 ± 0.16; -0.46 ± 0.16, respectively) and with overweight/obesity (n = 743; β ± SE = -0.59 ± 0.13; -0.50 ± 0.14, respectively), but not for those with diabetes (n = 187) or heart disease (n = 192). The HLS was not associated with CRP, after adjustment for potential confounders. Higher adherence to multiple lifestyle behaviors was associated with lower concentrations of inflammatory markers. Because low-grade inflammation may precede chronic diseases, following an overall healthy lifestyle may help lower risk of these diseases. Copyright © 2015 The Italian Society of Diabetology, the Italian Society for the Study of Atherosclerosis, the Italian Society of Human Nutrition, and the Department of Clinical Medicine and Surgery, Federico II

  7. Chronic Inflammatory Demyelinating Polyradiculoneuropathy: From Bench to Bedside

    PubMed Central

    Peltier, Amanda C.; Donofrio, Peter D.

    2015-01-01

    Chronic Inflammatory Demyelinating Polyradiculoneuropathy (CIDP) is the most common treatable chronic autoimmune neuropathy. Multiple diagnostic criteria have been established, with the primary goal of identifying neurophysiologic hallmarks of acquired demyelination. Treatment modalities have expanded to include numerous immuno-modulatory therapies, although the best evidence continues to be for corticosteroids, plasma exchange, and intravenous immunoglobulins (IVIg). This review describes the pathology, epidemiology, pathogenesis, diagnosis, and treatment of CIDP. PMID:23117943

  8. Chronic inflammatory demyelinating polyradiculoneuropathy: from bench to bedside.

    PubMed

    Peltier, Amanda C; Donofrio, Peter D

    2012-07-01

    Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is the most common treatable chronic autoimmune neuropathy. Multiple diagnostic criteria have been established, with the primary goal of identifying neurophysiologic hallmarks of acquired demyelination. Treatment modalities have expanded to include numerous immunomodulatory therapies, although the best evidence continues to be for corticosteroids, plasma exchange, and intravenous immunoglobulin (IVIg). This review describes the pathology, epidemiology, pathogenesis, diagnosis, and treatment of CIDP.

  9. Nutrition and chronic inflammatory rheumatic disease.

    PubMed

    Semerano, Luca; Julia, Chantal; Aitisha, Ouidade; Boissier, Marie-Christophe

    2016-11-30

    Nutrition is a major environmental influence on human health. Epidemiological and interventional studies suggest a pathophysiological or therapeutic role, respectively, for nutrition in inflammatory rheumatic diseases (IRDs). Nevertheless, the associations between nutrition and IRDs are often weak and inconsistent, and the available clinical trials on nutrition are methodologically flawed. Experimental evidence is accumulating that micronutrients in the diet may influence intestinal and systemic immune responses via complex interactions involving the gut microbiota. Micronutrients may, therefore, contribute to the pathogenesis of inflammatory diseases. No interventions targeting these interactions for diagnostic, prophylactic, or therapeutic purposes have been developed to date. Moreover, the relevance to human disease of experimental results obtained in animals or in vitro is unclear. Novel high-throughput technologies (-omics) may prove useful for a systems biology approach to these results that takes the complexity of the interactions into account. Concomitant cohort studies combining clinical and laboratory data collected over time may provide new impetus to research into the connections between nutrition and IRDs.

  10. Screening markers for chronic atrophic gastritis in Chiapas, Mexico.

    PubMed

    Ley, C; Mohar, A; Guarner, J; Herrera-Goepfert, R; Figueroa, L S; Halperin, D; Parsonnet, J

    2001-02-01

    Intestinal-type gastric adenocarcinomas usually are preceded by chronic atrophic gastritis. Studies of gastric cancer prevention often rely on identification of this condition. In a clinical trial, we sought to determine the best serological screening method for chronic atrophic gastritis and compared our findings to the published literature. Test characteristics of potential screening tests (antibodies to Helicobacter pyloni or CagA, elevated gastrin, low pepsinogen, increased age) alone or in combination were examined among consecutive subjects enrolled in a study of H. pylori and preneoplastic gastric lesions in Chiapas, Mexico; 70% had chronic atrophic gastritis. English-language articles concerning screening for chronic atrophic gastritis were also reviewed. Sensitivity for chronic atrophic gastritis was highest for antibodies to H. pylori (92%) or CagA, or gastrin levels >25 ng/l (both 83%). Specificity, however, was low for these tests (18, 41, and 22%, respectively). Pepsinogen levels were highly specific but insensitive markers of chronic atrophic gastritis (for pepsinogen I <25 microg/l, sensitivity was 6% and specificity was 100%; for pepsinogen I:pepsinogen II ratio <2.5, sensitivity was 14% and specificity was 96%). Combinations of markers did not improve test characteristics. Screening test characteristics from the literature varied widely and did not consistently identify a good screening strategy. In this study, CagA antibodies alone had the best combination of test characteristics for chronic atrophic gastritis screening. However, no screening test was both highly sensitive and highly specific for chronic atrophic gastritis.

  11. ‘I’m fishing really’ — inflammatory marker testing in primary care: a qualitative study

    PubMed Central

    Watson, Jessica; de Salis, Isabel; Hamilton, Willie; Salisbury, Chris

    2016-01-01

    Background Inflammatory markers can be helpful as part of the diagnostic workup for specific diseases or for monitoring disease activity. A third use is as a screening and/or triage tool to differentiate between the presence or absence of disease. Most research into inflammatory markers looks at diagnosis of specific diseases and comes from secondary care. Qualitative studies to explore when and why clinicians use these tests in primary care are lacking. Aim To identify clinicians’ approaches to inflammatory marker testing in primary care. Design and setting Qualitative study with 26 GPs and nurse practitioners. Method Interviews were conducted using a semi-structured topic guide. Clinicians reviewed recent cases of inflammatory marker testing in their pathology inbox. Interviews were audiorecorded and transcribed. Qualitative analysis was conducted by two of the authors. Results Clinicians are uncertain about the appropriate use of inflammatory markers and differ in their approach to testing patients with undifferentiated symptoms. Normal or significantly elevated inflammatory markers are seen as helpful, but mildly raised inflammatory markers in the context of non-specific symptoms are difficult to interpret. Clinicians describe a tension between not wanting to ‘miss anything’ and, on the other hand, being wary of picking up borderline abnormalities that can lead to cascades of further tests. Diagnostic uncertainty is a common reason for inflammatory marker testing, with the aim to reassure; however, paradoxically, inconclusive results can generate a cycle of uncertainty and anxiety. Conclusion Further research is needed to define when inflammatory marker testing is useful in primary care and how to interpret results. PMID:26852797

  12. 'I'm fishing really'--inflammatory marker testing in primary care: a qualitative study.

    PubMed

    Watson, Jessica; de Salis, Isabel; Hamilton, Willie; Salisbury, Chris

    2016-03-01

    Inflammatory markers can be helpful as part of the diagnostic workup for specific diseases or for monitoring disease activity. A third use is as a screening and/or triage tool to differentiate between the presence or absence of disease. Most research into inflammatory markers looks at diagnosis of specific diseases and comes from secondary care. Qualitative studies to explore when and why clinicians use these tests in primary care are lacking. To identify clinicians' approaches to inflammatory marker testing in primary care. Qualitative study with 26 GPs and nurse practitioners. Interviews were conducted using a semi-structured topic guide. Clinicians reviewed recent cases of inflammatory marker testing in their pathology inbox. Interviews were audiorecorded and transcribed. Qualitative analysis was conducted by two of the authors. Clinicians are uncertain about the appropriate use of inflammatory markers and differ in their approach to testing patients with undifferentiated symptoms. Normal or significantly elevated inflammatory markers are seen as helpful, but mildly raised inflammatory markers in the context of non-specific symptoms are difficult to interpret. Clinicians describe a tension between not wanting to 'miss anything' and, on the other hand, being wary of picking up borderline abnormalities that can lead to cascades of further tests. Diagnostic uncertainty is a common reason for inflammatory marker testing, with the aim to reassure; however, paradoxically, inconclusive results can generate a cycle of uncertainty and anxiety. Further research is needed to define when inflammatory marker testing is useful in primary care and how to interpret results. © British Journal of General Practice 2016.

  13. Chronic inflammatory demyelinating polyneuropathy after treatment with interferon-alpha.

    PubMed

    Hirotani, Makoto; Nakano, Hitoshi; Ura, Shigehisa; Yoshida, Kazuto; Niino, Masaaki; Yabe, Ichiro; Sasaki, Hidenao

    2009-01-01

    Interferon-alpha (IFN-alpha), though widely used for the treatment of chronic viral hepatitis, may be associated with the occurrence of autoimmune disorders. In this case report, a patient with chronic hepatitis C virus infection had chronic inflammatory demyelinating polyneuropathy (CIDP) after the initiation of IFN-alpha therapy. The neurological symptoms of this patient continued to progress even though the treatment with IFN-alpha had been withdrawn; the symptoms improved dramatically following treatment with intravenous immunoglobulin. This case may therefore provide an important clue to understand the immune mechanism of CIDP and IFN-alpha.

  14. Potential inflammatory markers in obstructive sleep apnea-hypopnea syndrome

    PubMed Central

    Lu, Dongmei; Li, Nanfang; Yao, Xiaoguang; Zhou, Ling

    2017-01-01

    Obstructive sleep apnea-hypopnea syndrome (OSAHS) is a complex chronic inflammatory respiratory disease with multiple pathogenic factors and high morbidity and mortality. Serum levels of nuclear factor-κB (NF-κB), hypoxia-inducible factor-1 alpha (HIF-1α), and surfactant protein D (SPD) were investigated in OSAHS patients, to determine their clinical significance and correlation with the pathogenesis. Patients were classified into a mild and moderate OSAHS group (n = 25) and severe OSAHS group (n = 33). Twenty healthy patients served as a control group. Peripheral blood levels of NF-κB, HIF-1α, and SPD were determined by Western blot, and a correlation analysis was performed. Severe OSAHS patients received nasal continuous positive airway pressure (nCPAP) therapy and were followed up after 2 months. NF-κB p65, HIF-1α, and SPD expression levels were determined after valid nCPAP therapy. NF-κB p65 and HIF-1α expression was significantly higher in severe OSAHS group than in the other two groups (p < 0.01), and was positively correlated with the apnea-hypopnea index (AHI) (r = 0.696, p < 0.001; r = 0.634, p < 0.001). SPD expression was significantly lower in severe OSAHS group than in the control group (p < 0.01) and mild and moderate OSAHS group (p < 0.01), and was negatively correlated with AHI (r = −0.569, p < 0.001). OSAHS pathogenesis was associated with changes in NF-κB, HIF-1α, and SPD protein expression levels. nCPAP therapy could improve the clinical characteristics of the patients, lower serum NF-κB and HIF-1α levels, and increase serum SPD levels. We conclude that OSAHS is related to the expression of NF-κB, HIF-1, and SPD. PMID:27754829

  15. Effect of magnesium sulfate and thyroxine on inflammatory markers in a rat model of hypothyroidism.

    PubMed

    Abbas, Amr M; Sakr, Hussein F

    2016-04-01

    Inflammation is a major risk factor for cardiovascular complications. Magnesium sulfate (MgSO4) has anti-inflammatory actions. Therefore we investigated the effects of levothyroxine and MgSO4 on inflammatory markers as C-reactive protein (CRP), interleukin-6, tumor necrosis factor-α (TNF-α), intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) in hypothyroid rats. Sixty male rats were divided into 6 groups; normal, normal + MgSO4, hypothyroidism, hypothyroidism + levothyroxine, hypothyroidism + MgSO4, and hypothyroidism + levothyroxine + MgSO4. Thyroxine, triiodothyronine, and thyroid-stimulating hormone (TSH), CRP, interleukin-6, TNF-α, ICAM-1, and VCAM-1 were measured in all rats. Hypothyroidism significantly increased TSH, CRP, interleukin-6, TNF-α, ICAM-1, and VCAM-1 and decreased triiodothronine and thyroxine. Treatment of hypothyroid rats with levothyroxine or MgSO4 significantly decreased CRP, interleukin-6, TNF-α, ICAM-1, and VCAM-1. Combined therapy of hypothyroid rats with levothyroxine and MgSO4 significantly decreased CRP, interleukin-6, TNF-α, ICAM-1, and VCAM-1 compared with hypothyroid rats either untreated or treated with levothyroxine or MgSO4. This study demonstrates that hypothyroid rats have chronic low grade inflammation, which may account for increased risk of cardiovascular diseases. Combined levothyroxine and MgSO4 is better than levothyroxine or MgSO4 alone in alleviating the chronic low grade inflammatory status and therefore reducing the risk of cardiovascular diseases in hypothyroid animals.

  16. Head mass in chronic pancreatitis: Inflammatory or malignant

    PubMed Central

    Dutta, Amit K; Chacko, Ashok

    2015-01-01

    Chronic pancreatitis increases the risk of developing pancreatic cancer. This often presents as a mass lesion in the head of pancreas. Mass lesion in the head of pancreas can also occur secondary to an inflammatory lesion. Recognising this is crucial to avoid unnecessary surgery. This is sometimes difficult as there is an overlap in clinical presentation and conventional computed tomography (CT) abdomen findings in inflammatory and malignant mass. Advances in imaging technologies like endoscopic ultrasound in conjunction with techniques like fine needle aspiration, contrast enhancement and elastography as well as multidetector row CT, magnetic resonance imaging and positron emission tomography scanning have been shown to help in distinguishing inflammatory and malignant mass. Research is ongoing to develop molecular techniques to help characterise focal pancreatic mass lesions. This paper reviews the current status of imaging and molecular techniques in differentiating a benign mass lesion in chronic pancreatitis and from malignancy. PMID:25789097

  17. Physical activity, by enhancing parasympathetic tone and activating the cholinergic anti-inflammatory pathway, is a therapeutic strategy to restrain chronic inflammation and prevent many chronic diseases.

    PubMed

    Lujan, Heidi L; DiCarlo, Stephen E

    2013-05-01

    Chronic diseases are the leading cause of death in the world and chronic inflammation is a key contributor to many chronic diseases. Accordingly, interventions that reduce inflammation may be effective in treating multiple adverse chronic conditions. In this context, physical activity is documented to reduce systemic low-grade inflammation and is acknowledged as an anti-inflammatory intervention. Furthermore, physically active individuals are at a lower risk of developing chronic diseases. However the mechanisms mediating this anti-inflammatory phenotype and range of health benefits are unknown. We hypothesize that the "cholinergic anti-inflammatory pathway" (CAP) mediates the anti-inflammatory phenotype and range of health benefits associated with physical activity. The CAP is an endogenous, physiological mechanism by which acetylcholine from the vagus nerve, interacts with the innate immune system to modulate and restrain the inflammatory cascade. Importantly, higher levels of physical activity are associated with enhanced parasympathetic (vagal) tone and lower levels of C-reactive protein, a marker of low-grade inflammation. Accordingly, physical activity, by enhancing parasympathetic tone and activating the CAP, may be a therapeutic strategy to restrain chronic inflammation and prevent many chronic diseases.

  18. [Fundamentals of chronic inflammatory lung diseases (asthma, COPD, fibrosis)].

    PubMed

    Roth, Michael

    2014-05-01

    Since three decades the prevalence of chronic inflammatory lung diseases (asthma, COPD, fibrosis) are worldwide increasing. In Switzerland about 5 % of the population develops asthma, while in other countries it affects up to 20 % (Maori: New Zealand). Today, asthma is the most frequent cause from absence from school and work, and significantly reduces life quality of the patients and their families. COPD, or the smoker's lung, is the 4th most frequent cause of death worldwide and in the Western society affects mainly cigarette smokers and ex-smokers, while in developing countries it is a diseases linked to open fire cocking with most patients being middle aged women. In both diseases only the symptoms can be controlled by muscle relaxing and anti-inflammatory drugs, but there is no cure available. The third chronic inflammatory lung disease is fibrosis which is increasing with the aging population. As indicated by the terminology "chronic inflammatory lung disease" it is widely assumed that the major cause of these diseases is chronic inflammation occurring in different segments of the lung. This hypothesis is now challenged as increasing evidence from clinical and experimental studies that suggest a much different pathogenesis. There is evidence that the inflammation may come second and tissue structural changes are already pre-set during embryogenesis and may become the major driver for the development of chronic inflammatory lung diseases later in life. The mechanism of this pre-disposition is largely unknown and the difficult to perform investigations have only started in recent years. This review aims to provide an overview of key studies published in the past 2 years on clinical and experimental research.

  19. Osteoporosis in chronic inflammatory disease: the role of malnutrition.

    PubMed

    Montalcini, Tiziana; Romeo, Stefano; Ferro, Yvelise; Migliaccio, Valeria; Gazzaruso, Carmine; Pujia, Arturo

    2013-02-01

    Osteoporosis is a metabolic bone disorder affecting million of people worldwide. Increased understanding of bone disease has led to a greater recognition of factors affecting bones, and consequently many secondary causes of osteoporosis were demonstrated. In this study, we aim to explore possible causes of bone loss and fractures in subjects affected by chronic inflammatory disease and to suggest new targets for intervention. In fact several studies, evaluated to perform this study, suggest that the patients with chronic inflammatory disease could be at high risk for fractures due to bone loss as consequence of malnutrition, caused by inflammation and hormonal change. Consequently, some actions could derive from the considerations of these mechanisms: a change in actual approach of chronic patients, that may include the investigation on the possible presence of osteoporosis, as well as further research on this topic to find a better therapy to prevent osteoporosis considering all the mechanisms described.

  20. Dissociated sterol-based liver X receptor agonists as therapeutics for chronic inflammatory diseases.

    PubMed

    Yu, Shan; Li, Sijia; Henke, Adam; Muse, Evan D; Cheng, Bo; Welzel, Gustav; Chatterjee, Arnab K; Wang, Danling; Roland, Jason; Glass, Christopher K; Tremblay, Matthew

    2016-07-01

    Liver X receptor (LXR), a nuclear hormone receptor, is an essential regulator of immune responses. Activation of LXR-mediated transcription by synthetic agonists, such as T0901317 and GW3965, attenuates progression of inflammatory disease in animal models. However, the adverse effects of these conventional LXR agonists in elevating liver lipids have impeded exploitation of this intriguing mechanism for chronic therapy. Here, we explore the ability of a series of sterol-based LXR agonists to alleviate inflammatory conditions in mice without hepatotoxicity. We show that oral treatment with sterol-based LXR agonists in mice significantly reduces dextran sulfate sodium colitis-induced body weight loss, which is accompanied by reduced expression of inflammatory markers in the large intestine. The anti-inflammatory property of these agonists is recapitulated in vitro in mouse lamina propria mononuclear cells, human colonic epithelial cells, and human peripheral blood mononuclear cells. In addition, treatment with LXR agonists dramatically suppresses inflammatory cytokine expression in a model of traumatic brain injury. Importantly, in both disease models, the sterol-based agonists do not affect the liver, and the conventional agonist T0901317 results in significant liver lipid accumulation and injury. Overall, these results provide evidence for the development of sterol-based LXR agonists as novel therapeutics for chronic inflammatory diseases.-Yu, S., Li, S., Henke, A., Muse, E. D., Cheng, B., Welzel, G., Chatterjee, A. K., Wang, D., Roland, J., Glass, C. K., Tremblay, M. Dissociated sterol-based liver X receptor agonists as therapeutics for chronic inflammatory diseases. © FASEB.

  1. Systemic Inflammatory Markers Are Closely Associated with Atherogenic Lipoprotein Subfractions in Patients Undergoing Coronary Angiography

    PubMed Central

    Zhang, Yan; Li, Sha; Xu, Rui-Xia; Zhu, Cheng-Gang; Guo, Yuan-Lin; Wu, Na-Qiong; Sun, Jing; Li, Jian-Jun

    2015-01-01

    Objective. To investigate the relationship between inflammatory markers and atherogenic lipoprotein subfractions. Methods. We studied 520 eligible subjects who were not receiving any lipid-lowering therapy. The inflammatory markers including white blood cell (WBC) count, high-sensitivity C-reactive protein (hs-CRP), fibrinogen, erythrocyte sedimentation rate (ESR), and D-dimer were measured. A multimarker inflammatory index was developed. Low-density lipoprotein (LDL) and high-density lipoprotein (HDL) separation processes were performed using Lipoprint System. Results. In age- and sex-adjusted analysis, several inflammatory markers (WBC count, hs-CRP, fibrinogen, and ESR) were positively related to circulating non-HDL cholesterol and remnant cholesterol (p < 0.05, all). Among lipoprotein subfractions, we observed a positive association of inflammatory markers with very low-density lipoprotein cholesterol, small LDL cholesterol, and LDL score (p < 0.05, all). Meanwhile, a negative association was detected between inflammatory markers and mean LDL particle size (p < 0.05) or large HDL cholesterol (p < 0.05). Moreover, we found that the relationships between multimarker index quartiles and small LDL cholesterol, LDL score, and mean LDL particle size were slightly stronger in patients with CAD. Conclusions. Systemic inflammatory markers are positively correlated with small LDL cholesterol and LDL score while being negatively linked with mean LDL particle size and large HDL cholesterol, highlighting the potential contribution to increased cardiovascular risk. PMID:26688615

  2. Macrolide Therapy in Chronic Inflammatory Diseases

    PubMed Central

    Kwiatkowska, Brygida; Maślińska, Maria

    2012-01-01

    Macrolides are a group of antibiotics with a distinctive macrocyclic lactone ring combined with sugars (cladinose, desosamine). The action of macrolides is to block protein synthesis by binding to the subunit of 50S ribosome of bacteria. Prototype macrolide was erythromycin, which came into clinical practice in the 50s of the 20th century. Its antimicrobial spectrum covers the scope of the penicillins but is extended to the impact of atypical bacteria. In the 90s more drugs of this group were synthesized—they have less severe side effects than erythromycin, extended spectrum of Gram-negative bacteria. Macrolides are effective in treating mycobacterial infections especially in patients infected with HIV. It is now known that in addition to antibacterial abilities, macrolides have immunomodulatory effects—they inhibit the production of proinflammatory cytokines (TNF, IL1, 6, and 8) affect transcription factors (NF-κB) as well as costimulaton (CD 80) and adhesion molecules (ICAM). This review article focused not only on the their antimicrobial abilities but also on efficacy in the treatment of several inflammatory disorders independent of the infectious agent. Their wider use as immunomodulators requires further study, which can lead to an extension of indications for their administration. PMID:22969171

  3. Glycosaminoglycan sulodexide modulates inflammatory pathways in chronic venous disease.

    PubMed

    Mannello, F; Ligi, D; Raffetto, J D

    2014-06-01

    Inflammation represents an important epiphenomenon in the etiopathogenesis of chronic venous disease, a worldwide debilitating condition affecting millions of subjects. The pathophysiology of chronic venous disease (CVD) is based on the hemodynamic abnormalities in conjunction to alterations in cellular and extracellular matrix biocompounds. The endothelial dysfunction results from early perturbation in the endothelium linked to glycocalyx injury and promoted by inflammatory cells and mediators (such as matrix metalloproteinases and interleukins), which lead to progressive dilation of the vein resulting in chronic venous insufficiency. Activated leukocytes during the inflammatory process release enzymes, free radicals, chemokines and inflammatory cytokines in the vessel microenvironment, which are responsible for the changes of the venous wall and venous valve, reflux and venous hypertension, and the development/progression of tissue destruction and skin changes. Sulodexide, a highly purified mixture of glycosaminoglycans composed by 80% fast moving heparin and 20% of dermatan sulphate, exhibits anti-thrombotic and profibrinolytic properties, restoring also the essential endothelial glycocalyx. Glycosaminoglycan sulodexide has been also characterized to reduce the release of inflammatory cytokines/chemokines and to inhibit the matrix metalloproteinases-related proteolytic cascades, counteracting endothelial dysfunctions. The pleiotropic effects of sulodexide set the basis for a very promising agent in treating the spectrum of CVD.

  4. Endomorphins as agents for the treatment of chronic inflammatory disease.

    PubMed

    Jessop, David S

    2006-01-01

    Endomorphin (EM)-1 and EM-2 are tetrapeptides located within the mammalian central nervous system and immune tissues, with high affinity and specificity for micro-opioid receptors. Most of the literature has focused on the analgesic properties of EM-1 and EM-2 in animal models of neuropathic or neurogenic pain, but there is persuasive evidence emerging that EMs can also exert potent anti-inflammatory effects in both acute and chronic peripheral inflammation. The purpose of this review is to present and evaluate the evidence for anti-inflammatory properties of EM-1 and EM-2 with a view to their potential for use in chronic human inflammatory disease. Distribution of EMs within the immune system and functional roles as immunomodulatory agents are summarized and discussed. Possible milestones to be met revolve around issues of peptide stability, biodegradability problems and optimal route and method of delivery. The potential for delivery of a low-cost drug with both peripheral anti-inflammatory and analgesic properties, effective in low doses, and targeted to the site of inflammation, should focus our attention on further development of EMs as potent therapeutic agents in chronic inflammation.

  5. Childhood chronic inflammatory demyelinating polyneuropathy with nonuniform pathologic features.

    PubMed

    Luan, Xinghua; Zheng, Riliang; Chen, Bin; Yuan, Yun

    2010-08-01

    Nonuniform pathologic changes in chronic inflammatory demyelinating polyneuropathy were previously reported only in adult humans. We analyzed the pathologic features of 12 children, aged 2-17 years, with chronic inflammatory demyelinating polyneuropathy. Six patients manifested a preceding illness. Five patients presented a chronic, monophasic course, and seven presented a relapsing-remitting course. Three patients exhibited multiple cranial-nerve involvement. Five of 12 (41.7%) patients presented nonuniform features. Two subtypes of nonuniform lesions were revealed. One exhibited varying myelinated fiber content between nerve fascicles, and one exhibited onion bulbs involving a variable number of fascicles. Macrophages were evident in 11 patients, and the number of CD3-positive T cells in the nonuniform group was greater compared with the uniform group (P = 0.045). Our results demonstrate that childhood chronic inflammatory demyelinating polyneuropathy exhibits pathologically nonuniform features, thus providing more evidence to assist in differential diagnoses of pediatric patients. However, clinical and electrophysiologic features, as well as responses to treatment, were similar in the nonuniform and uniform groups.

  6. Novel inflammatory markers for incident pre-diabetes and type 2 diabetes: the Rotterdam Study.

    PubMed

    Brahimaj, Adela; Ligthart, Symen; Ghanbari, Mohsen; Ikram, Mohammad Arfan; Hofman, Albert; Franco, Oscar H; Kavousi, Maryam; Dehghan, Abbas

    2017-03-01

    The immune response involved in each phase of type 2 diabetes (T2D) development might be different. We aimed to identify novel inflammatory markers that predict progression from normoglycemia to pre-diabetes, incident T2D and insulin therapy. We used plasma levels of 26 inflammatory markers in 971 subjects from the Rotterdam Study. Among them 17 are novel and 9 previously studied. Cox regression models were built to perform survival analysis.

  7. GCF Resistin As A Novel Marker in Patients with Chronic Periodontitis and Rheumatoid Arthritis.

    PubMed

    Mittal, Manoj; Hassan, Basit; Desai, Khushboo; Duseja, Shilpa; Kumar, Santosh; Reddy, Sharaschandra G

    2015-04-01

    The associational studies between periodontitis and rheumatoid arthritis are less documented, although they are found to have similar inflammatory pathogenesis. Resistin, a novel adipokine is suggested to be a common link between periodontitis and rheumatoid arthritis. The aim of the present study was to reinforce the inter-relationship between periodontitis and rheumatoid arthritis by using resistin as a potent inflammatory marker. Hundred patients (aged >30 y) of either sex were selected for this study and were divided equally into four groups of 25 patients each. Group A consisted of healthy individuals, Group B consisted of patients with chronic periodontitis, Group C of patients with rheumatoid arthritis and Group D had patients suffering from both arthritis and periodontitis. Periodontal parameters assessed were plaque index (PI), modified gingival index (GI) and probing depth (PD). Panoramic radiographs were taken to confirm the diagnosis of periodontitis. Rheumatoid arthritis was confirmed by the rheumatologists and seropositivity for rheumatoid factor (RF) was checked. Resistin levels were analysed in GCF collected from all the four groups and statistical analysis was done by using Pearson correlation coefficient. The GCF of all the patients showed presence of resistin. The level of resistin was highest in Group D patients and least in Group A patients. On analysing the samples together positive co-relation was found between GCF resistin and PD, PI, GI and RF. Resistin levels are increased in both chronic periodontitis and rheumatoid arthritis. Therefore, the increased level of GCF resistin can be regarded as potential inflammatory marker for periodontitis and rheumatoid arthritis.

  8. Lactobacillus plantarum CECT 7315/7316 intake modulates the acute and chronic innate inflammatory response.

    PubMed

    Vilahur, Gemma; López-Bernal, Sergi; Camino, Sandra; Mendieta, Guiomar; Padró, Teresa; Badimon, Lina

    2015-10-01

    Probiotics may confer health benefits for the host. Although Lactobacillus has demonstrated to stimulate the immune response, only a few strains have demonstrated immunomodulatory properties. The newly identified Lactobacillus plantarum strains CECT7315 and CECT7316 (LP3457) seem to boost the immune system in individuals that immune decline. We aimed to investigate whether LP3457 protects against inflammation and the mechanism behind. LP3457 potential anti-inflammatory effects were assessed in an acute model LPS-induced inflammation in healthy rats and in a chronic model of low-grade inflammation in Zucker diabetic fatty (ZDF) rats. Wistar rats received LP3457 or placebo control for 20 days. Lipopolysaccharide (LPS; 1 mg/kg) was injected intraperitoneally at day 14, and animals were sacrificed 6 days after. Blood was collected at baseline (day 0) and consecutively at day 7, 14, 17, and 20 for haematological evaluation and assessment of anti-inflammatory/pro-inflammatory systemic markers. Myeloperoxidase activity was investigated in the ileum. ZDF rats received LP3457 or placebo control during 8 weeks, and changes in inflammasome-related transcripts were assessed in the ileum. LPS induced a comparable and significant leucocytosis 3 days post-injection (day 17) in both LP3457-treated and LP3457-untreated rats. However, the probiotic supplementation attenuated IL-1β, IL-6, and CRP release and increased anti-inflammatory IL-10 levels 6 days post-LPS induction (p < 0.05 vs. placebo). LP3457-supplemented animals also displayed lower intestinal myeloperoxidase activity (p < 0.05 vs. placebo). Chronic administration of LP3457 to ZDF rats resulted in a significant downregulation of the inflammasome signalling pathway (p < 0.05 vs. placebo). Intake of LP3457 attenuates both acute endotoxemia-induced and chronic metabolically induced inflammatory reactions and the inflammasome signalling pathway. The stabilization and regulation of the gut microbiota is an important target

  9. Inflammatory and immune markers associated with physical frailty syndrome: findings from Singapore longitudinal aging studies

    PubMed Central

    Lu, Yanxia; Tan, Crystal Tze Ying; Nyunt, Ma Shwe Zin; Mok, Esther Wing Hei; Camous, Xavier; Kared, Hassen; Fulop, Tamas; Feng, Liang

    2016-01-01

    Chronic systematic inflammation and reduced immune system fitness are considered potential contributing factors to the development of age-related frailty, but the underlying mechanisms are poorly defined. This exploratory study aimed to identify frailty-related inflammatory markers and immunological phenotypes in a cohort of community-dwelling adults aged ≥ 55 years. Frailty was assessed using two models, a Frailty Index and a categorical phenotype, and correlated with levels of circulating immune biomarkers and markers of senescence in immune cell subsets. We identified eight serological biomarkers that were associated with frailty, including sgp130, IL-2Rα, I-309, MCP-1, BCA-1, RANTES, leptin, and IL-6R. Frailty Index was inversely predicted by the frequency of CD3+, CD45RA+, and central memory CD4 cells, and positively predicted by the loss of CD28 expression, especially in CD8+ T cells, while frailty status was predicted by the frequency of terminal effector CD8+ T cells. In γ/δ T cells, frailty was negatively associated with CD27, and positively associated with IFNγ+TNFα- secretion by γ/δ2+ cells and IFNγ-TNFα+ secretion by γ/δ2- cells. Increased numbers of exhausted and CD38+ B cells, as well as CD14+CD16+ inflammatory monocytes, were also identified as frailty-associated phenotypes. This pilot study supports an association between inflammation, cellular immunity, and the process of frailty. These findings have significance for the early identification of frailty using circulating biomarkers prior to clinical manifestations of severe functional decline in the elderly. PMID:27119508

  10. CIRCULATING INFLAMMATORY MARKERS IN POLYCYSTIC OVARY SYNDROME: A SYSTEMATIC REVIEW AND META-ANALYSIS

    PubMed Central

    Escobar-Morreale, Héctor F.; Luque-Ramírez, Manuel; González, Frank

    2010-01-01

    Objective To review and meta-analyse the studies evaluating the status of serum inflammatory markers in women with Polycystic Ovary Syndrome (PCOS). Design Systematic review and meta-analysis of articles published in English before January 2010 and identified using the Entrez-PubMed engine. Setting Academic hospital Interventions Measurement of serum concentrations of inflammatory markers by high-sensitivity techniques. Main Outcome Measures Meta-analyses of the mean difference in serum C-reactive protein (CRP), interlekin-6 (IL-6) and tumor necrosis factor-α (TNF-α) concentrations among patients with PCOS and appropriate controls, applying random-effects models to limit interstudy variability, and using appropriate estimates of evidence dissemination bias. Results Meta-analysis of the 31 articles meeting inclusion criteria showed that circulating CRP was 96% higher in women with PCOS compared to controls (95% confidence interval 71% – 122%, z = 7.32, p < 0.0001) without evidence dissemination bias (Egger’s regression intercept 0.45, 95% confidence interval −2.30 – 3.21, P = 0.739). These findings persisted after excluding five studies with mismatches in body mass and/or frequency of obesity between women with PCOS and controls. Meta-analyses involving 10 studies of IL-6, and 9 studies of TNF-α revealed no statistically significant differences between PCOS and controls. Conclusion Women with PCOS exhibit elevation in circulating CRP that is independent of obesity. This finding corroborates existing molecular evidence of the chronic low-grade inflammation that may underpin the pathogenesis of this disorder. PMID:21168133

  11. Prognostic markers and stratification of chronic lymphocytic leukemia.

    PubMed

    Furman, Richard R

    2010-01-01

    Chronic lymphocytic leukemia (CLL) is one of the most common lymphoid malignancies and is characterized by a tremendously variable clinical course. Additionally, whereas the median age at diagnosis is 72 years, CLL is diagnosed with increasing frequency in younger patients. Given the toxicities associated with currently available therapies, being able to predict which patients will need treatment could play a significant role in preserving bone marrow function and reducing morbidity and mortality. While a great many prognostic markers have been identified that predict outcomes for patients with CLL. Learning how to use these prognostic markers to provide patient care is more difficult.

  12. Chronic inflammatory demyelinating polyneuropathy associated with primary biliary cirrhosis.

    PubMed

    Murata, Ken-ya; Ishiguchi, Hiroshi; Ando, Ryuki; Miwa, Hideto; Kondo, Tomoyoshi

    2013-12-01

    We report a patient with chronic inflammatory demyelinating polyneuropathy associated with primary biliary cirrhosis (PBC). Except for minimal biochemical abnormalities, clinical symptoms of PBC were not observed, and we diagnosed our patient with asymptomatic PBC from the results of a liver biopsy. Although the patient noticed little muscle weakness, an electrophysiological study demonstrated slow conduction velocities and prolonged distal latencies, with definite conduction blocks in the median, ulnar, and tibial nerves. The disturbed sensory pattern was asymmetrical, and sensory nerve action potentials were not evoked. From these observations, we diagnosed this patient with chronic inflammatory demyelinating polyneuropathy. Neuropathy associated with PBC is very rare. We must differentiate demyelinating neuropathy with PBC in patients with asymmetrical sensory dominant neuropathy with high immunoglobulin M titers, and investigate for the presence of anti-mitochondrial antibodies to rule out a complication of asymptomatic PBC.

  13. [Chronic inflammatory bowel disease--pathogenic concepts and therapeutic perspectives].

    PubMed

    Madsen, J R

    2000-03-06

    Chronic inflammatory bowel disease (IBD) is considered to be a consequence of inappropriate upregulation of immune reactions evoked by the colonic microflora. Abnormalities observed in IBD may be explained, at least in part, by an unfavourable balance between pro- and anti-inflammatory cytokines. Conventional drug treatment of IBD may soon be replaced by more selective inhibitors that act centrally in the inflammatory process. Immunoneutralisation with chimeric anti-tumour necrosis factor-alpha (TNF alpha) antibodies reduces treatment refractory IBD, including fistular Chrons' disease, but recombinant human TNF alpha-receptor fusion proteins may be equally effective with potentially fewer side effects. This view also applies to chimeric antibodies directed against cytokines or adhesion molecules. Potentially more promising are antisense oligonucleotides and matrix-metalloproteinase inhibitors. Whether sustained remission can be achieved probably depends on successful unravelling of the aetiology of IBD.

  14. Pro-Inflammatory Markers in Relation to Cardiovascular Disease in HIV Infection. A Systematic Review

    PubMed Central

    Vos, Alinda G.; Idris, Nikmah S.; Barth, Roos E.; Klipstein-Grobusch, Kerstin; Grobbee, Diederick E.

    2016-01-01

    Background In the past years many inflammatory markers have been studied in association with clinically manifest cardiovascular disease (CVD) and carotid intima-media thickness (CIMT) in HIV-infected patients, to obtain insights in the increased cardiovascular risk observed in HIV infection. This systematic review provides an oversight of the current knowledge. Methods A search was performed in PubMed, Embase and Cochrane in July 2014, identifying all articles from 1996 onwards addressing the relation between inflammatory markers and CVD or CIMT in HIV-positive adults. Two authors, using predefined criteria, independently conducted the selection of articles, critical appraisal and extraction of the data. Analysis was focused on the immune markers that were most frequently assessed. The review protocol was registered in the PROSPERO database at 11 July 2014 (registration number CRD42014010516). This review was performed according to the PRISMA guideline. Findings Forty articles were selected; eight addressing cardiovascular disease (CVD) and thirty-two addressing CIMT. C-reactive protein (CRP), interleukin-6 (IL-6) and d-dimer were assessed most frequently in relation to the occurrence of CVD; in four out of eight studies. All three markers were positively related to CVD in three out of four studies. Studies addressing CIMT were too heterogeneous with respect to patient populations, inflammatory markers, CIMT measurement protocols and statistical methods to allow for a formal meta-analysis to obtain summary statistics. CRP, IL-6 and soluble vascular cell adhesion molecule (sVCAM-1) were the most studied markers in relation to CIMT. None of the inflammatory markers showed an association with CIMT. Interpretation This review showed a relation between some inflammatory markers and CVD, however, no consistent relation is observed for CIMT. Statistical approaches that yields effect estimates and standardized CIMT protocols should be chosen. Further research should focus

  15. Phospholipid transfer protein activity is associated with inflammatory markers in patients with cardiovascular disease.

    PubMed

    Cheung, Marian C; Brown, B Greg; Marino Larsen, Emily K; Frutkin, Andrew D; O'Brien, Kevin D; Albers, John J

    2006-01-01

    Plasma phospholipid lipid transfer protein (PLTP) has several known key functions in lipoprotein metabolism. Recent studies suggest that it also may play a role in the inflammatory response. Inflammatory cell activity contributes to the development of atherosclerosis. To seek further evidence for the association of PLTP with inflammation, we studied the relationship between PLTP activity and five inflammatory markers [C-reactive protein (CRP), serum amyloid A (SAA), interleukin 6 (IL-6), white blood cells (WBC), and fibrinogen] in 93 patients with low HDL and cardiovascular disease (CVD). Plasma PLTP activity had the strongest correlation with CRP (r=0.332, P<0.001) followed by SAA (r=0.239, P=0.021). PLTP, CRP, and SAA were significantly associated with body mass index (BMI), insulin or glucose, apolipoprotein (apo) B, and/or apo E level (r=0.264-0.393, P<0.01). PLTP, SAA, and IL-6 also were associated with the concentration of HDL particles without apo A-II [Lp(A-I)](r=0.373-0.472, P<0.005, n=56), but not particles with apo A-II. Smoking was associated with increased PLTP activity, CRP, and WBC, and hypertension with increased PLTP activity. In linear models, CRP remained significantly associated with PLTP after adjustment of CVD risk factors and insulin resistance. Also, much of the variability of plasma PLTP activity was explained by CRP, BMI, Lp(A-I), smoking, glucose, and blood pressure. These findings show for the first time that plasma PLTP activity is associated positively with CRP in CVD, a state of chronic inflammation.

  16. Sulfur Mustard (SM) Lesions in Organ-Cultured Human Skin: Markers of Injury and Inflammatory Mediators

    DTIC Science & Technology

    1988-03-01

    second, but more cumbersome, way to assess injury to human skin explants is the interference with the incorporation of [14C]leucine by the epidermal cells ...assayed for markers of cell death and early inflammatory media- tors. Lactic dehydrogenase (LDE), angiotensin-converting enzyme (ACE), trypsin-like and...markers for injury produced by SM. ACE is a marker for endo- thelial damage. Lysosomal enzymes participate in cell autolysis. We did, however, find one

  17. Targeted anti-inflammatory therapeutics in asthma and chronic obstructive lung disease

    PubMed Central

    Durham, Andrew L.; Caramori, Gaetano; Chung, Kian F.; Adcock, Ian M.

    2016-01-01

    Asthma and chronic obstructive pulmonary disease (COPD) are chronic inflammatory diseases of the airway, although the drivers and site of the inflammation differ between diseases. Asthmatics with a neutrophilic airway inflammation are associated with a poor response to corticosteroids, whereas asthmatics with eosinophilic inflammation respond better to corticosteroids. Biologicals targeting the Th2-eosinophil nexus such as anti–interleukin (IL)-4, anti–IL-5, and anti–IL-13 are ineffective in asthma as a whole but are more effective if patients are selected using cellular (eg, eosinophils) or molecular (eg, periostin) biomarkers. This highlights the key role of individual inflammatory mediators in driving the inflammatory response and for accurate disease phenotyping to allow greater understanding of disease and development of patient-oriented antiasthma therapies. In contrast to asthmatic patients, corticosteroids are relatively ineffective in COPD patients. Despite stratification of COPD patients, the results of targeted therapy have proved disappointing with the exception of recent studies using CXC chemokine receptor (CXCR)2 antagonists. Currently, several other novel mediator-targeted drugs are undergoing clinical trials. As with asthma specifically targeted treatments may be of most benefit in specific COPD patient endotypes. The use of novel inflammatory mediator-targeted therapeutic agents in selected patients with asthma or COPD and the detection of markers of responsiveness or nonresponsiveness will allow a link between clinical phenotypes and pathophysiological mechanisms to be delineated reaching the goal of endotyping patients. PMID:26334389

  18. Targeted anti-inflammatory therapeutics in asthma and chronic obstructive lung disease.

    PubMed

    Durham, Andrew L; Caramori, Gaetano; Chung, Kian F; Adcock, Ian M

    2016-01-01

    Asthma and chronic obstructive pulmonary disease (COPD) are chronic inflammatory diseases of the airway, although the drivers and site of the inflammation differ between diseases. Asthmatics with a neutrophilic airway inflammation are associated with a poor response to corticosteroids, whereas asthmatics with eosinophilic inflammation respond better to corticosteroids. Biologicals targeting the Th2-eosinophil nexus such as anti-interleukin (IL)-4, anti-IL-5, and anti-IL-13 are ineffective in asthma as a whole but are more effective if patients are selected using cellular (eg, eosinophils) or molecular (eg, periostin) biomarkers. This highlights the key role of individual inflammatory mediators in driving the inflammatory response and for accurate disease phenotyping to allow greater understanding of disease and development of patient-oriented antiasthma therapies. In contrast to asthmatic patients, corticosteroids are relatively ineffective in COPD patients. Despite stratification of COPD patients, the results of targeted therapy have proved disappointing with the exception of recent studies using CXC chemokine receptor (CXCR)2 antagonists. Currently, several other novel mediator-targeted drugs are undergoing clinical trials. As with asthma specifically targeted treatments may be of most benefit in specific COPD patient endotypes. The use of novel inflammatory mediator-targeted therapeutic agents in selected patients with asthma or COPD and the detection of markers of responsiveness or nonresponsiveness will allow a link between clinical phenotypes and pathophysiological mechanisms to be delineated reaching the goal of endotyping patients.

  19. Inflammatory markers following acute fuel oil exposure or bacterial lipopolysaccharide in mallard ducks (Anas platyrhynchos).

    PubMed

    Lee, Kelly A; Tell, Lisa A; Mohr, F Charles

    2012-12-01

    Adult mallard ducks (Anas platyrhynchos) were orally dosed with bunker C fuel oil for 5 days, and five different inflammatory markers (haptoglobin, mannan-binding lectin, ceruloplasmin, unsaturated iron-binding capacity, and plasma iron) were measured in blood plasma prior to and 8, 24, 48, and 72 hr following exposure. In order to contrast the response to fuel oil with that of a systemic inflammatory response, an additional five ducks were injected intramuscularly with bacterial lipopolysaccharide (LPS). Oil-treated birds had an inflammatory marker profile that was significantly different from control and LPS-treated birds, showing decreases in mannan-binding lectin-dependent hemolysis and unsaturated iron-binding capacity, but no changes in any of the other inflammatory markers. Birds treated with oil also exhibited increased liver weights, decreased body and splenic weights, and decreased packed cell volume.

  20. F2-isoprostanes in kidney transplant patients: relationship with inflammatory markers.

    PubMed

    Lauzurica, R; Pastor, M C; Bayés, B; Hernández, J M; Bonet, J; Llopis, M A; Carrera, L; Romero, R

    2005-11-01

    This prospective study evaluated the relationship between inflammation and oxidative stress in a group of dialysis patients just before and 3 months after kidney transplantation and compared the results with a control group of healthy subjects. The oxidative stress markers determined were different F2-isoprostane isomers. The inflammatory markers included C-reactive protein, interleukin-6, tumor necrosis factor-alpha, and pregnancy-associated plasma protein A. Forty-three patients were the study group and 50 healthy subjects from a hospital blood bank as controls. The results showed levels of inflammatory and oxidative stress markers to be higher in the dialysis patients than in the control group, although they improved following kidney transplantation. Finally, significant correlations were observed between F2-isoprostane isomers and inflammatory markers.

  1. Chronic venous disease - Part I: Inflammatory biomarkers in wound healing.

    PubMed

    Ligi, Daniela; Mosti, Giovanni; Croce, Lidia; Raffetto, Joseph D; Mannello, Ferdinando

    2016-10-01

    Venous leg ulcers (VLUs) produce wound fluid (WF), as a result of inflammatory processes within the wound. It is unclear if WF from different healing phases of VLU has a peculiar biochemical profile and how VLU microenvironment affects the wound healing mechanisms. This study was conducted to evaluate the cytokine/chemokine profiles in WF from distinct VLU phases, in WF- and LPS-stimulated monocytes and treated with glycosaminoglycan Sulodexide, a therapeutic option for VLU healing. WF and plasma were collected from patients with VLU during active inflammatory (Infl) and granulating (Gran) phases. Demographics, clinical characteristics and pain measurements were evaluated. WF, plasma, and THP-1 supernatants were analyzed for 27 inflammatory mediators by multiplex immunoassay. Our results demonstrated that: 1) pain was significantly increased in patients with Infl compared to Gran VLU; 2) cytokine profile of Infl WF was found to be statistically different from that Gran WF, as well significantly increased respect to plasma; 3) LPS- and WF-stimulation of THP-1 cells significantly increased the expression of several cytokines compared to untreated cells; 4) Sulodexide treatment of both LPS- and WF-stimulated THP-1 monocytes was able to significantly down-regulate the release of peculiar inflammatory mediators. Our study highlighted the importance to understand biomolecular processes underlying CVI when providing treatment for chronic VLU. Identification of inflammatory biomarkers in leg ulcer microenvironment, may provide useful tools for predicting healing outcome and developing targeted therapies. Copyright © 2016 Elsevier B.V. All rights reserved.

  2. Novel immunotherapeutic strategies in chronic inflammatory demyelinating polyneuropathy.

    PubMed

    Mathis, Stéphane; Vallat, Jean-Michel; Magy, Laurent

    2016-02-01

    Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is a chronic immune-mediated neuropathy: it is clinically heterogeneous (relapsing-remitting form, chronic progressive form, monophasic form or CIDP having a Guillain-Barré syndrome-like onset), but potentially treatable. Although its pathophysiology remains largely unknown, CIDP is considered an immune-mediated neuropathy. Therefore, many immunotherapies have been proposed in this peripheral nervous system disorder, the most known efficient treatments being intravenous immunoglobulin, corticosteroids and plasma exchange. However, these therapies remain unsatisfactory for many patients, so numerous other immunotherapeutic strategies have been evaluated, based on their immunosuppressant or immunomodulatory potency. We have performed a large review of the literature about treatment in CIDP, with a special emphasis on novel and alternative immunotherapeutic strategies.

  3. Inflammatory markers are elevated in overweight Mexican-American children

    USDA-ARS?s Scientific Manuscript database

    The purpose of the present study was to determine the effect of body weight on blood lipid profile, insulin resistance, and inflammatory biomarkers in Mexican-American children. Children (13.3 +/- 0.1 year) were recruited from a local school and assigned to one of three groups as a volunteer sample...

  4. Silymarin suppresses basal and stimulus-induced activation, exhaustion, differentiation, and inflammatory markers in primary human immune cells.

    PubMed

    Lovelace, Erica S; Maurice, Nicholas J; Miller, Hannah W; Slichter, Chloe K; Harrington, Robert; Magaret, Amalia; Prlic, Martin; De Rosa, Stephen; Polyak, Stephen J

    2017-01-01

    Silymarin (SM), and its flavonolignan components, alter cellular metabolism and inhibit inflammatory status in human liver and T cell lines. In this study, we hypothesized that SM suppresses both acute and chronic immune activation (CIA), including in the context of HIV infection. SM treatment suppressed the expression of T cell activation and exhaustion markers on CD4+ and CD8+ T cells from chronically-infected, HIV-positive subjects. SM also showed a trend towards modifying CD4+ T cell memory subsets from HIV+ subjects. In the HIV-negative setting, SM treatment showed trends towards suppressing pro-inflammatory cytokines from non-activated and pathogen-associated molecular pattern (PAMP)-activated primary human monocytes, and non-activated and cytokine- and T cell receptor (TCR)-activated mucosal-associated invariant T (MAIT) cells. The data suggest that SM elicits broad anti-inflammatory and immunoregulatory activity in primary human immune cells. By using novel compounds to alter cellular inflammatory status, it may be possible to regulate inflammation in both non-disease and disease states.

  5. Silymarin suppresses basal and stimulus-induced activation, exhaustion, differentiation, and inflammatory markers in primary human immune cells

    PubMed Central

    Lovelace, Erica S.; Maurice, Nicholas J.; Miller, Hannah W.; Slichter, Chloe K.; Harrington, Robert; Magaret, Amalia; Prlic, Martin; De Rosa, Stephen; Polyak, Stephen J.

    2017-01-01

    Silymarin (SM), and its flavonolignan components, alter cellular metabolism and inhibit inflammatory status in human liver and T cell lines. In this study, we hypothesized that SM suppresses both acute and chronic immune activation (CIA), including in the context of HIV infection. SM treatment suppressed the expression of T cell activation and exhaustion markers on CD4+ and CD8+ T cells from chronically-infected, HIV-positive subjects. SM also showed a trend towards modifying CD4+ T cell memory subsets from HIV+ subjects. In the HIV-negative setting, SM treatment showed trends towards suppressing pro-inflammatory cytokines from non-activated and pathogen-associated molecular pattern (PAMP)-activated primary human monocytes, and non-activated and cytokine- and T cell receptor (TCR)-activated mucosal-associated invariant T (MAIT) cells. The data suggest that SM elicits broad anti-inflammatory and immunoregulatory activity in primary human immune cells. By using novel compounds to alter cellular inflammatory status, it may be possible to regulate inflammation in both non-disease and disease states. PMID:28158203

  6. Aortic Intima-Media Thickness as an Early Marker of Atherosclerosis in Children With Inflammatory Bowel Disease.

    PubMed

    Aloi, Marina; Tromba, Luciana; Rizzo, Valentina; D'Arcangelo, Giulia; Dilillo, Anna; Blasi, Sara; Civitelli, Fortunata; Kiltzanidi, Dimitra; Redler, Adriano; Viola, Franca

    2015-07-01

    The aims of this study were to determine the presence of endothelial dysfunction by measuring aortic intima-media thickness (aIMT) and carotid intima-media thickness (cIMT) and to evaluate the role of traditional risk factors for premature atherosclerosis in children with inflammatory bowel disease (IBD). Thirty-four children with IBD (25 Crohn disease [CD] and 9 ulcerative colitis [UC]; mean age 11.1 years) and 27 healthy subjects matched for sex and age were enrolled. In all of the patients, demographic characteristics and risk factors for atherosclerosis (age, sex, body mass index, blood pressure, dyslipidemia, active and passive smoking, and family history for cardiovascular diseases), CD and UC clinical activity scores, and inflammatory markers were evaluated. aIMT and cIMT were measured by high-resolution B-mode ultrasound. aIMT was significantly higher in patients than in controls (P < 0.0005). No significant differences were found for cIMT, although the carotid thickness was higher in patients with IBD than in healthy subjects. At a univariate analysis, inflammatory markers levels and tobacco smoking exposure were significantly related to higher aIMT values, whereas in a multivariate regression model, the inflammatory status was the only independent variable correlated with high aIMT. aIMT is an earlier marker of preclinical atherosclerosis than cIMT in young children with active IBD. The inflammatory status and the smoking exposure are significantly correlated with the premature endothelial dysfunction. These data emphasize the importance of controlling the chronic intestinal inflammation and endorsing smoke-free environments for children and adolescents with IBD.

  7. Rethinking the triggering inflammatory processes of chronic periaortitis.

    PubMed

    Meier, Pascal; Vogt, Bruno; Blanc, Edouard

    2007-01-01

    Chronic periaortitis (CP) is an uncommon inflammatory disease which primarily involves the infrarenal portion of the abdominal aorta. However, CP should be regarded as a generalized disease with three different pathophysiological entities, namely idiopathic retroperitoneal fibrosis (RPF), inflammatory abdominal aortic aneurysm and perianeurysmal RPF. These entities share similar histopathological characteristics and finally will lead to fibrosis of the retroperitoneal space. Beside fibrosis, an infiltrate with variable chronic inflammatory cell is present. The majority of these cells are lymphocytes and macrophages as well as vascular endothelial cells, most of which are HLA-DR-positive. B and T cells are present with a majority of T cells of the T-helper phenotype. Cytokine gene expression analysis shows the presence of interleukin (IL)-1alpha, IL-2, IL-4, interferon-gamma and IL-2 receptors. Adhesion molecules such as E-selectin, intercellular adhesion molecule-1 and the vascular cell adhesion molecule-1 were also found in aortic tissue, and may play a significant role in CP pathophysiology. Although CP pathogenesis remains unknown, an exaggerated inflammatory response to advanced atherosclerosis (ATS) has been postulated to be the main process. Autoimmunity has also been proposed as a contributing factor based on immunohistochemical studies. The suspected allergen may be a component of ceroid, which is elaborated within the atheroma. We review the pathogenesis and the pathophysiology of CP, and its potential links with ATS. Clinically relevant issues are summarized in each section with regard to the current working hypothesis of this complex inflammatory disease. Copyright 2007 S. Karger AG, Basel.

  8. Chemical castration in cattle with intratesticular injection of sodium chloride: Effects on stress and inflammatory markers.

    PubMed

    Oliveira, Fernando C; Ferreira, Carlos E R; Haas, Cristina S; Oliveira, Leonardo G; Mondadori, Rafael G; Schneider, Augusto; Rovani, Monique T; Gonçalves, Paulo B D; Vieira, Arnaldo D; Gasperin, Bernardo G; Lucia, Thomaz

    2017-03-01

    Intratesticular injection (ITI) of sodium chloride (NaCl) is efficient for chemical castration of young calves, but its effects on calves welfare are unknown. Two experiments were conducted to evaluate the effects of ITI of 20% NaCl on stress and inflammatory markers in calves less than 20 days old and to assess the efficiency of ITI of 30% NaCl in 5 months old calves. In Experiment 1, control calves were only restrained and compared to calves submitted to castration through surgery (SC) and ITI with 20% NaCl (n = 9/group). No differences were observed for the eye corner temperature measured by thermography from 60 s before to 60 s after the procedures (P > 0.05). In the SC group, acute serum cortisol levels increased at 30 and 60 min after the procedure, but increased levels in the ITI group occurred only at 30 min (P < 0.05). Chronic discomfort markers were measured at 0, 24, 48, 72 and 96 h after the procedures (D0, D1, D2, D3 and D4, respectively). The serum levels of the paraoxonase 1 (PON1) enzyme and cortisol did not differ among groups (P > 0.05). Scrotal temperature was higher at D1 in the SC group than for the other groups, but lowest at D4 compared to the control (both P < 0.05). In Experiment 2, histological sections of testes were compared after ITI with either 30% NaCl or 30% calcium chloride (CaCl2), to intact calves (control). After 60 days, intact seminiferous tubules and mediastinum were observed after ITI with 30% NaCl, whereas coagulative necrosis, inflammatory infiltration and calcification occurred after ITI with 30% CaCl2. Efficient chemical castration through ITI of 20% NaCl in young calves was followed by slight stress and inflammatory responses compared to surgical castration. However, ITI of 30% NaCl was ineffective for chemical castration of 5 months old calves. Copyright © 2016 Elsevier Inc. All rights reserved.

  9. [Chronic inflammatory bowel diseases. Clinical aspects and new therapy approaches].

    PubMed

    Siegmund, B

    2012-11-01

    There is a continuously increasing incidence in inflammatory bowel diseases affecting mostly young people who are in a vulnerable phase of life. Thus, early diagnosis and initiation of an effective therapeutic regimen is critical in order to maintain a good quality of life. In Germany, the standard therapeutic strategy is an accelerated step up approach, including the introduction of early immunosuppressive therapy if required. Although novel therapeutic strategies have found their way into clinical use there is still a substantial subgroup of patients where effective therapy is lacking. The future introduction of anti-adhesion molecule antibodies might provide a realistic option for this subgroup. Equally important is the availability of predictive markers allowing stratification of patients into subgroups at the time of diagnosis. Assuming that the CD8(+) T cell transcriptome approach will be confirmed in prospective trials, personalized therapy in patients with inflammatory bowel disease will be the next step.

  10. Increase of inflammatory markers after indoor renovation activities: the LISA birth cohort study.

    PubMed

    Herberth, Gunda; Gubelt, Reinhild; Röder, Stefan; Krämer, Ursula; Schins, Roel P F; Diez, Ulrike; Borte, Michael; Heinrich, Joachim; Wichmann, H-Erich; Herbarth, Olf; Lehmann, Irina

    2009-09-01

    There is concern about indoor air quality as a possible cause for health impairment. Exposure to indoor renovation activities has been shown to be associated with airway symptoms and allergic manifestations in children. The aim of this study is to analyse immune markers responsible for disease development in relation to renovation activities. Within the LISAplus (Life style Immune System Allergy) birth cohort study, blood samples of 6-yr-old children were analysed for concentration of the inflammatory markers interleukin (IL)-8, IL-6, tumour necrosis factor-alpha, MCP-1 and IL-10. Data on indoor renovation activities (painting, flooring, new furniture) were assessed with a questionnaire filled in by the parents. Data on cytokine blood concentrations and exposure variables were available for 250 children. Increased levels of IL-8 and MCP-1 in children's blood were related to renovation activities. In particular, new floor covering was associated with increased inflammatory markers. Among floor covering materials only wall-to-wall carpets were associated with elevated IL-8 and Monocyte Chemoattractant Protein-1 (MCP-1) levels. No association between the single renovation activities painting and furnishing and blood concentration of inflammatory markers has been found. Our data shows that IL-8 and MCP-1 may be suitable markers for monitoring inflammatory reactions in relation with renovation activities. Among renovation activities floor covering seems to induce the strongest inflammatory reactions.

  11. IVIG regulates BAFF expression in patients with chronic inflammatory demyelinating polyneuropathy (CIDP).

    PubMed

    Ritter, Christian; Förster, Dominik; Albrecht, Philipp; Hartung, Hans-Peter; Kieseier, Bernd C; Lehmann, Helmar C

    2014-09-15

    Recent studies indicate that the cytokine B-cell activating factor (BAFF) is involved in the pathogenesis of chronic inflammatory demyelinating polyneuropathy (CIDP). Intravenous immunoglobulin (IVIg) is standard treatment for CIDP and is known to rapidly modulate increased serum levels of pro-inflammatory cytokines. We evaluated the expression profile of BAFF and its corresponding BAFF-receptor in samples from CIDP patients, focusing on rapid changes before and after IVIg treatment. In CIDP patients BAFF serum concentrations were elevated compared to controls. Treatment with high-dose IVIg restored those elevated BAFF serum levels. Whereas treatment with IVIg did not affect BAFF production in monocytes, antibodies against BAFF could be detected in IVIg preparations, which may explain the short-term decrease of BAFF levels after IVIg treatment. Our data suggest that BAFF plays an important role in the pathogenesis of CIDP and may serve as marker for IVIg treatment response.

  12. [Renal amyloidosis complicating the outcome of chronic inflammatory colitis].

    PubMed

    Béji, Soumaya; Kaaroud, Hayet; Ben Moussa, Fatma; Goucha, Rym; Abderrahim, Ezzedine; El Younsi, Fethi; Ben Maïz, Hédi

    2004-07-31

    In 4 patients we observed the association of an amyloid nephropathy and a chronic inflammatory bowel disease (Crohn's' disease in 3 cases and ulcerative rectocolitis in 1 case). These patients, aged a mean of 37 years (range: 28-48 years), had been admitted for exploration of a nephrotic syndrome associated with renal failure in 2 cases. The investigations lead to the diagnosis of AA type amyloidosis in the 4 cases. One patient was lost from follow-up. One patient was treated with salazopyrine, one with corticosteroids and one with colchicine. After a mean follow-up of 16 months (5-30 months), all the patients had persistent nephrotic syndrome, with end stage renal failure in one case, persistence of normal renal function in one case and improved renal function in one case. None of the patients exhibited remission in the nephrotic syndrome. The response of amyloidosis to the treatment of the chronic inflammatory bowel disease varied. Corticosteroids and colchicine stabilised renal function in 2 of our patients but without remission in the nephrotic syndrome. AA amyloidosis is a rare complication of inflammatory bowel disease. The indication for colchicine is important to consider particularly since the response of amyloidosis to the treatment of the causal disease does not, in the majority of cases, lead to the remission of the amyloidosis, the prognosis of which is determined by the extent of renal involvement.

  13. SOCS1 Mimetic Peptide Suppresses Chronic Intraocular Inflammatory Disease (Uveitis)

    PubMed Central

    He, Chang; Yu, Cheng-Rong; Mattapallil, Mary J.; Sun, Lin

    2016-01-01

    Uveitis is a potentially sight-threatening disease characterized by repeated cycles of remission and recurrent inflammation. The JAK/STAT pathway regulates the differentiation of pathogenic Th1 and Th17 cells that mediate uveitis. A SOCS1 mimetic peptide (SOCS1-KIR) that inhibits JAK2/STAT1 pathways has recently been shown to suppress experimental autoimmune uveitis (EAU). However, it is not clear whether SOCS1-KIR ameliorated uveitis by targeting JAK/STAT pathways of pathogenic lymphocytes or via inhibition of macrophages and antigen-presenting cells that also enter the retina during EAU. To further investigate mechanisms that mediate SOCS1-KIR effects and evaluate the efficacy of SOCS1-KIR as an investigational drug for chronic uveitis, we induced EAU in rats by adoptive transfer of uveitogenic T-cells and monitored disease progression and severity by slit-lamp microscopy, histology, and optical coherence tomography. Topical administration of SOCS1-KIR ameliorated acute and chronic posterior uveitis by inhibiting Th17 cells and the recruitment of inflammatory cells into retina while promoting expansion of IL-10-producing Tregs. We further show that SOCS1-KIR conferred protection of resident retinal cells that play critical role in vision from cytotoxic effects of inflammatory cytokines by downregulating proapoptotic genes. Thus, SOCS1-KIR suppresses uveitis and confers neuroprotective effects and might be exploited as a noninvasive treatment for chronic uveitis. PMID:27703302

  14. Effects of resistance training at different loads on inflammatory markers in young adults.

    PubMed

    Forti, Louis Nuvagah; Van Roie, Evelien; Njemini, Rose; Coudyzer, Walter; Beyer, Ingo; Delecluse, Christophe; Bautmans, Ivan

    2017-03-01

    Suppressing inflammaging at an early stage in life via exercise might prevent chronic diseases later in life. The aim was to investigate the influence of resistance training at different external loads on inflammatory markers in healthy young adults. Serum was collected for basal levels of cytokines (IL-1beta, IL-6, IL-8, sTNFR1, IL-1RA, IL-10 and GM-CSF) before and after 9 weeks exercise from 36 young (22 ± 2 years) healthy subjects who were randomized to three times weekly supervised resistance training at either HImax (n = 12, 1 × 10-12 repetitions at 80% 1RM), LO (n = 12, 1 × 10-12 repetitions at 40% 1RM), or LOmax (n = 12, 1 × 10-12 repetitions at 40% 1RM preceded by 60 repetitions at 20-25% 1RM) respectively. Overall, IL-8 increased (p < 0.001) and IL-6 decreased (p = 0.001) after training, but no significant time*group interaction was found (respectively, p = 0.283 and p = 0.058 for IL-8 and IL-6). When analyzed separately, IL-8 increased significantly in HImax (p = 0.022) and LOmax (p = 0.024); and IL-6 decreased significantly in LOmax (p = 0.009) and LO (p = 0.013). No significant overall time effect was observed for sTNFR1 and IL-1RA; however, in HImax sTNFR1 (p = 0.031) and IL-1RA (p = 0.014) increased significantly, but remained unchanged in LOmax and LO. IL-1beta, IL-10 and GM-CSF levels remained undetectable in most participants. Nine weeks of resistance training-irrespective of the external load-have beneficial effects on circulating IL-8 and IL-6. In addition, training at high external load increases the anti-inflammatory cytokines sTNFR1 and IL-1RA. The results of this study show that resistance training has anti-inflammatory effects in healthy young persons and that the response of the different inflammatory mediators depends on the magnitude of the external load.

  15. Chronic inflammatory demyelinating polyradiculoneuropathy: from pathology to phenotype

    PubMed Central

    Mathey, Emily K; Park, Susanna B; Hughes, Richard A C; Pollard, John D; Armati, Patricia J; Barnett, Michael H; Taylor, Bruce V; Dyck, P James B; Kiernan, Matthew C; Lin, Cindy S-Y

    2015-01-01

    Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is an inflammatory neuropathy, classically characterised by a slowly progressive onset and symmetrical, sensorimotor involvement. However, there are many phenotypic variants, suggesting that CIDP may not be a discrete disease entity but rather a spectrum of related conditions. While the abiding theory of CIDP pathogenesis is that cell-mediated and humoral mechanisms act together in an aberrant immune response to cause damage to peripheral nerves, the relative contributions of T cell and autoantibody responses remain largely undefined. In animal models of spontaneous inflammatory neuropathy, T cell responses to defined myelin antigens are responsible. In other human inflammatory neuropathies, there is evidence of antibody responses to Schwann cell, compact myelin or nodal antigens. In this review, the roles of the cellular and humoral immune systems in the pathogenesis of CIDP will be discussed. In time, it is anticipated that delineation of clinical phenotypes and the underlying disease mechanisms might help guide diagnostic and individualised treatment strategies for CIDP. PMID:25677463

  16. Accelerated atherosclerosis in patients with chronic inflammatory rheumatologic conditions

    PubMed Central

    Hong, Jison; Maron, David J; Shirai, Tsuyoshi; Weyand, Cornelia M

    2015-01-01

    Atherosclerosis is a complex inflammatory disease involving aberrant immune and tissue healing responses, which begins with endothelial dysfunction and ends with plaque development, instability and rupture. The increased risk for coronary artery disease in patients with rheumatologic diseases highlights how aberrancy in the innate and adaptive immune system may be central to development of both disease states and that atherosclerosis may be on a spectrum of immune-mediated conditions. Recognition of the tight association between chronic inflammatory disease and complications of atherosclerosis will impact the understanding of underlying pathogenic mechanisms and change diagnostic and therapeutic approaches in patients with rheumatologic syndromes as well as patients with coronary artery disease. In this review, we provide a summary of the role of the immune system in atherosclerosis, discuss the proposed mechanisms of accelerated atherosclerosis seen in association with rheumatologic diseases, evaluate the effect of immunosuppression on atherosclerosis and provide updates on available risk assessment tools, biomarkers and imaging modalities. PMID:27042216

  17. [Chronic obstructive pulmonary disease (COPD): expression of a chronic inflammatory reaction].

    PubMed

    Ziesche, Rolf

    2005-03-01

    Our understanding of chronic inflammation in COPD has been profoundly changed as a result of findings which suggest that airway inflammation in COPD consists not only of a chronic cellular inflammatory reaction dominated by lymphocytes and neutrophil granulocytes, but also of an intensified secondary wound healing reaction. Unfortunately, little is known about the impact of both reactions on the maintenance of chronic airway inflammation in COPD. Systematic biological evaluation under clinical circumstances will be necessary in order to realize new therapeutic options in COPD.

  18. Inflammatory and Metabolic Alterations of Kager's Fat Pad in Chronic Achilles Tendinopathy.

    PubMed

    Pingel, Jessica; Petersen, M Christine H; Fredberg, Ulrich; Kjær, Søren G; Quistorff, Bjørn; Langberg, Henning; Hansen, Jacob B

    2015-01-01

    Achilles tendinopathy is a painful inflammatory condition characterized by swelling, stiffness and reduced function of the Achilles tendon. Kager's fat pad is an adipose tissue located in the area anterior to the Achilles tendon. Observations reveal a close physical interplay between Kager's fat pad and its surrounding structures during movement of the ankle, suggesting that Kager's fat pad may stabilize and protect the mechanical function of the ankle joint. The aim of this study was to characterize whether Achilles tendinopathy was accompanied by changes in expression of inflammatory markers and metabolic enzymes in Kager's fat pad. A biopsy was taken from Kager's fat pad from 31 patients with chronic Achilles tendinopathy and from 13 healthy individuals. Gene expression was measured by reverse transcription-quantitative PCR. Focus was on genes related to inflammation and lipid metabolism. Expression of the majority of analyzed inflammatory marker genes was increased in patients with Achilles tendinopathy compared to that in healthy controls. Expression patterns of the patient group were consistent with reduced lipolysis and increased fatty acid β-oxidation. In the fat pad, the pain-signaling neuropeptide substance P was found to be present in one third of the subjects in the Achilles tendinopathy group but in none of the healthy controls. Gene expression changes in Achilles tendinopathy patient samples were consistent with Kager's fat pad being more inflamed than in the healthy control group. Additionally, the results indicate an altered lipid metabolism in Kager's fat pad of Achilles tendinopathy patients.

  19. The dilemma of diabetes in chronic inflammatory demyelinating polyneuropathy

    PubMed Central

    Bril, Vera; Blanchette, Christopher M.; Noone, Joshua M.; Runken, M. Chris; Gelinas, Deborah; Russell, James W.

    2017-01-01

    Purpose We reviewed the literature on chronic inflammatory demyelinating polyneuropathy (CIDP) in diabetes mellitus (DM) and explored real-world data on the prevalence and treatment of CIDP within DM. Methods: A literature search of Scopus was performed for the terms chronic inflammatory demyelinating polyradiculoneuropathy, chronic inflammatory demyelinating polyneuropathy, CIDP, and prevalence, incidence, epidemiology, or diabetes; peripheral neuropathy and prevalence or diabetes. We also searched through the reference lists of the resulting publications for additional findings that may have been missed. Additional publications on guidelines for the diagnosis of CIDP and diabetic neuropathy were also included. A descriptive analysis of the 2009–2013 PharMetrics Plus™ Database was performed to estimate the prevalence and treatment of CIDP within the DM population. Results There is an increasing body of literature suggesting that the prevalence of CIDP tends to be higher in diabetic patients, especially in those of older age. Our real-world data seem to support published findings from the literature. For the total cohort (N = 101,321,694), the percent prevalence of CIDP (n = 8,173) was 0.008%; DM (n = 4,026,740) was 4%. The percent prevalence of CIDP without DM (n = 5,986) was 0.006%; CIDP with DM (n = 2,187) was 9-fold higher at 0.054%. For patients >50 years old, there was a significantly higher percentage of CIDP with DM than CIDP without DM. Approximately 50% of CIDP patients were treated with IVIg, 23%–24% with steroids, 1%–2% with PE, and 20%–23% received no treatment. Conclusions In addition to the growing evidence of higher prevalence of CIDP in DM, our findings reinforce the need for heightened awareness of the association of CIDP and DM. PMID:27389526

  20. Associations between sleep quality and inflammatory markers in patients with schizophrenia.

    PubMed

    Fang, Shih-Hua; Suzuki, Katsuhiko; Lim, Chin Leong; Chung, Ming-Shun; Ku, Po-Wen; Chen, Li-Jung

    2016-12-30

    Sleep disorder is a risk factor for several systemic inflammation-related diseases and there are extensive data showing that schizophrenia is associated with chronic low-grade systemic inflammation. This study investigated the associations between sleep quality and inflammatory markers in patients with schizophrenia, which has not been examined before. Sleep quality (total sleep time, sleep efficiency, sleep onset latency, total activity counts, wake after sleep onset, number of awakening, and average length of awakening) was measured using actigraphy in 199 schizophrenia inpatients. The state of inflammation was measured using blood concentration of white blood cells (WBC) and neutrophils, together with neutrophil-lymphocyte ratio (NLR), and platelet-lymphocyte ratio (PLR). The results showed that total sleep time was negatively associated with NLR and PLR, and sleep efficiency was negatively associated with neutrophil counts and NLR. Sleep onset latency, total activity counts, wake after sleep onset, and number of awakening were positively associated with WBC and neutrophil counts. The average length of awakening was positively associated with NLR and PLR. This is the first report to suggest that improving sleep quality may modulate the state of inflammation in patients with schizophrenia.

  1. Chronic recurrent multifocal osteomyelitis and inflammatory bowel disease.

    PubMed

    Audu, Grace K; Nikaki, Kornilia; Crespi, Daniel; Spray, Christine; Epstein, Jenny

    2015-05-01

    Chronic recurrent multifocal osteomyelitis (CRMO) has been reported in association with inflammatory bowel disease (IBD), mostly in children. We describe the UK paediatric experience of CRMO and IBD and review the global literature. Three cases of CRMO and IBD were identified in UK children during the last 10 years. This adds to the previously published 24 cases worldwide (15 children). We provide further evidence for the true association of CRMO and IBD, and a greater understanding of disease course. CRMO may be considered a rare extraintestinal complication of IBD.

  2. Ocular Neuromyotonia Associated with Chronic Inflammatory Demyelinating Polyneuropathy.

    PubMed

    Kung, Nathan H; Bucelli, Robert C; McClelland, Collin M; Van Stavern, Gregory P

    2015-10-01

    Ocular neuromyotonia (ONM) is a neuro-ophthalmic disorder characterized by episodic diplopia caused by contraction of one or more ocular muscles due to spontaneous excitation of the respective ocular motor nerve. We report a patient whose ocular neuromyotonia arose in the setting of a subacute demyelinating polyneuropathy consistent with chronic inflammatory demyelinating polyneuropathy (CIDP) and subsequently resolved following the initiation of intravenous immunoglobulin (IVIg) for her neuropathy. Our patient provides additional evidence towards the role of demyelination and ephaptic neurotransmission in ocular neuromyotonia and also represents the first reported case of ocular neuromyotonia associated with a systemic neurological condition.

  3. Autoantibodies against vinculin in patients with chronic inflammatory demyelinating polyneuropathy.

    PubMed

    Beppu, Minako; Sawai, Setsu; Satoh, Mamoru; Mori, Masahiro; Kazami, Takahiro; Misawa, Sonoko; Shibuya, Kazumoto; Ishibashi, Masumi; Sogawa, Kazuyuki; Kado, Sayaka; Kodera, Yoshio; Nomura, Fumio; Kuwabara, Satoshi

    2015-10-15

    To identify the target molecules of chronic inflammatory demyelinating polyneuropathy (CIDP), we used proteomic-based approach in the extracted proteins from porcine cauda equina. Two of 31 CIDP patients had markedly elevated serum autoantibodies against vinculin, a cell adhesion protein. Both of the patients with anti-vinculin antibodies had similar clinical manifestation, which are compatible with those of "typical" CIDP. Immunocytochemistry showed that vinculin was stained at the myelin sheath of the sciatic nerves by serum samples. Our results suggest that vinculin is a possible immunological target molecule in a subpopulation of typical CIDP patients.

  4. Gene expression changes in chronic inflammatory demyelinating polyneuropathy skin biopsies.

    PubMed

    Puttini, Stefania; Panaite, Petrica-Adrian; Mermod, Nicolas; Renaud, Susanne; Steck, Andreas J; Kuntzer, Thierry

    2014-05-15

    Chronic-inflammatory demyelinating polyneuropathy (CIDP) is an immune-mediated disease with no known biomarkers for diagnosing the disease or assessing its prognosis. We performed transcriptional profiling microarray analysis on skin punch biopsies from 20 CIDP patients and 17 healthy controls to identify disease-associated gene expression changes. We demonstrate changes in expression of genes involved in immune and chemokine regulation, growth and repair. We also found a combination of two upregulated genes that can be proposed as a novel biomarker of the disorder.

  5. Treatment of chronic relapsing inflammatory polyradiculoneuropathy by plasma exchange.

    PubMed

    Server, A C; Lefkowith, J; Braine, H; McKhann, G M

    1979-09-01

    A 58-year-old man developed recurrent episodes of symmetrical motor weakness associated with acroparesthesias and areflexia. The cerebrospinal fluid protein was elevated and nerve conduction velocities were slowed. There was no evidence of systemic disease or toxic exposure, and a diagnosis of chronic relapsing inflammatory polyradiculoneuropathy was made. The patient improved during treatment with corticosteroids, but steroid-induced complications necessitated discontinuance. A recrudescence of symptoms prompted a search for alternative therapy, and plasma exchange was tried. A marked improvement in strength was noted following each course of plasma exchange, suggesting that further similar trials are justified.

  6. Reconstruction magnetic resonance neurography in chronic inflammatory demyelinating polyneuropathy.

    PubMed

    Shibuya, Kazumoto; Sugiyama, Atsuhiko; Ito, Sho-ichi; Misawa, Sonoko; Sekiguchi, Yukari; Mitsuma, Satsuki; Iwai, Yuta; Watanabe, Keisuke; Shimada, Hitoshi; Kawaguchi, Hiroshi; Suhara, Tetsuya; Yokota, Hajime; Matsumoto, Hiroshi; Kuwabara, Satoshi

    2015-02-01

    To study distribution and patterns of nerve hypertrophy in chronic inflammatory demyelinating polyneuropathy (CIDP), magnetic resonance neurography with 3-dimensional reconstruction of short tau inversion recovery images was performed in 33 patients. This technique clearly showed longitudinal morphological changes from the cervical roots to the nerve trunks in the proximal arm. Nerve enlargement was detected in 88% of the patients. According to the clinical subtype of CIDP, typical CIDP patients showed symmetric and root-dominant hypertrophy, whereas Lewis-Sumner syndrome patients had multifocal fusiform hypertrophy in the nerve trunks. The patterns of nerve hypertrophy presumably reflect the different pathophysiology of each CIDP subtype.

  7. Emerging risk factors and markers of chronic kidney disease progression.

    PubMed

    Kronenberg, Florian

    2009-12-01

    Chronic kidney disease (CKD) is a common condition with an increasing prevalence. A number of comorbidities are associated with CKD and prognosis is poor, with many patients experiencing disease progression. Recognizing the factors associated with CKD progression enables high-risk patients to be identified and given more intensive treatment if necessary. The identification of new predictive markers might improve our understanding of the pathogenesis and progression of CKD. This Review discusses a number of emerging factors and markers for which epidemiological evidence from prospective studies indicates an association with progression of CKD. The following factors and markers are discussed: asymmetric dimethylarginine, factors involved in calcium-phosphate metabolism, adrenomedullin, A-type natriuretic peptide, N-terminal pro-brain natriuretic peptide, liver-type fatty acid binding protein, kidney injury molecule 1, neutrophil gelatinase-associated lipocalin, apolipoprotein A-IV, adiponectin and some recently identified genetic polymorphisms. Additional epidemiological and experimental data are required before these markers can be broadly used for the prediction of CKD progression and before the risk factors can be considered as potential drug targets in clinical interventional trials.

  8. [Special surgical complications in chronic inflammatory bowel diseases].

    PubMed

    Kroesen, A J

    2015-04-01

    After colorectal and anorectal interventions for chronic inflammatory bowel diseases, specific complications can occur.In Crohn's disease these complications mainly occur after proctocolectomy. Pelvic sepsis can be prevented by omentoplasty with fixation inside the pelvis. A persisting sepsis of the sacral cavity can be treated primarily by dissection of the anal sphincter which ensures better drainage. In cases of chronic sacral sepsis, transposition of the gracilis muscle is a further effective option. Early recurrence of a transsphincteric anal fistula should be treated by reinsertion of a silicon seton drainage.Complications after restorative proctocolectomy are frequent and manifold (35%). The main acute complications are anastomotic leakage and pelvic sepsis. Therapy consists of transperineal drainage of the abscess with simultaneous transanal drainage. Late complications due to technical and septic reasons are still a relevant problem even 36 years after introduction of this operative technique. A consistent approach with detailed diagnostic and surgical therapy results in a 75% rescue rate of ileoanal pouches.

  9. Acute restraint stress induces specific changes in nitric oxide production and inflammatory markers in the rat hippocampus and striatum.

    PubMed

    Chen, Hsiao-Jou Cortina; Spiers, Jereme G; Sernia, Conrad; Lavidis, Nickolas A

    2016-01-01

    Chronic mild stress has been shown to cause hippocampal neuronal nitric oxide synthase (NOS) overexpression and the resultant nitric oxide (NO) production has been implicated in the etiology of depression. However, the extent of nitrosative changes including NOS enzymatic activity and the overall output of NO production in regions of the brain like the hippocampus and striatum following acute stress has not been characterized. In this study, outbred male Wistar rats aged 6-7 weeks were randomly allocated into 0 (control), 60, 120, or 240 min stress groups and neural regions were cryodissected for measurement of constitutive and inducible NOS enzymatic activity, nitrosative status, and relative gene expression of neuronal and inducible NOS. Hippocampal constitutive NOS activity increased initially but was superseded by the inducible isoform as stress duration was prolonged. Interestingly, hippocampal neuronal NOS and interleukin-1β mRNA expression was downregulated, while the inducible NOS isoform was upregulated in conjunction with other inflammatory markers. This pro-inflammatory phenotype within the hippocampus was further confirmed with an increase in the glucocorticoid-antagonizing macrophage migration inhibitory factor, Mif, and the glial surveillance marker, Ciita. This indicates that despite high levels of glucocorticoids, acute stress sensitizes a neuroinflammatory response within the hippocampus involving both pro-inflammatory cytokines and inducible NOS while concurrently modulating the immunophenotype of glia. Furthermore, there was a delayed increase in striatal inducible NOS expression while no change was found in other pro-inflammatory mediators. This suggests that short term stress induces a generalized increase in inducible NOS signaling that coincides with regionally specific increased markers of adaptive immunity and inflammation within the brain.

  10. The role and utility of faecal markers in inflammatory bowel disease

    PubMed Central

    Lehmann, Frank S.; Burri, Emanuel

    2015-01-01

    Crohn’s disease and ulcerative colitis are characterized by periods of symptomatic relapse and remission. Diagnosis and assessment of inflammatory bowel disease has so far been based on clinical evaluation, serum parameters, radiology and endoscopy. Faecal markers such as calprotectin or lactoferrin have emerged as new diagnostic tools to detect and monitor intestinal inflammation. This review focuses on their potential clinical applications and limitations in the management of inflammatory bowel disease. PMID:25553077

  11. The Immune Protective Effect of the Mediterranean Diet against Chronic Low-grade Inflammatory Diseases

    PubMed Central

    Casas, Rosa; Sacanella, Emilio; Estruch, Ramon

    2016-01-01

    Dietary patterns high in refined starches, sugar, and saturated and trans-fatty acids, poor in natural antioxidants and fiber from fruits, vegetables, and whole grains, and poor in omega-3 fatty acids may cause an activation of the innate immune system, most likely by excessive production of proinflammatory cytokines associated with a reduced production of anti-inflammatory cytokines. The Mediterranean Diet (MedDiet) is a nutritional model inspired by the traditional dietary pattern of some of the countries of the Mediterranean basin. This dietary pattern is characterized by the abundant consumption of olive oil, high consumption of plant foods (fruits, vegetables, pulses, cereals, nuts and seeds); frequent and moderate intake of wine (mainly with meals); moderate consumption of fish, seafood, yogurt, cheese, poultry and eggs; and low consumption of red meat, processed meat products and seeds. Several epidemiological studies have evaluated the effects of a Mediterranean pattern as protective against several diseases associated with chronic low-grade inflammation such as cancer, diabetes, obesity, atherosclerosis, metabolic syndrome and cognition disorders. The adoption of this dietary pattern could counter the effects of several inflammatory markers, decreasing, for example, the secretion of circulating and cellular biomarkers involved in the atherosclerotic process. Thus, the aim of this review was to consider the current evidence about the effectiveness of the MedDiet in these chronic inflammatory diseases due to its antioxidant and anti-inflammatory properties, which may not only act on classical risk factors but also on inflammatory biomarkers such as adhesion molecules, cytokines or molecules related to the stability of atheromatic plaque. PMID:25244229

  12. Effect of acute thermal injury in status of serum vitamins, inflammatory markers, and oxidative stress markers: preliminary data.

    PubMed

    Vinha, Paula Pileggi; Martinez, Edson Zangiacomi; Vannucchi, Helio; Marchini, Julio Sergio; Farina, Jayme Adriano; Jordao, Alceu Afonso; Cunha, Selma Freire

    2013-01-01

    The objective of this study was to evaluate the vitamin status, inflammatory markers, and oxidative stress markers in adult patients up to 3 days after thermal injury. This prospective study was conducted with 11 patients 24 to 72 hours after thermal injury (Burn Group), total surface area ranging from 10 to 41%, 34.3 ± 9.3 years, 82% of males, body mass index of 22.3 ± 2.9 kg/m(2). We included 11 healthy adults (Control Group), 36.5 ± 7.6 years, 73% of males, and body mass index of 23.8 ± 2.5 kg/m(2). Laboratory data were measured (plasma total protein, albumin, transferrin, lymphocyte counts, zinc, and iron), as well as serum vitamins (folic acid, vitamin B12, and vitamins A, C, and E), inflammatory stress markers (C-reactive protein, ferritin, and acid α1-glycoprotein) and oxidative stress markers such as glutathione peroxidase (GPx) and thiobarbituric acid reactive substances. The inflammatory stress was characterized by lower levels of total protein (median difference 1.2 g/dL, 95% CI: 0.4-2.1) and albumin (median difference 0.9 g/dL, 95% CI: 0.5-1.5), and higher levels of C-reactive protein (median difference -8.12 mg/dL, 95% CI: -11.62 to 4.61) and α-1 glycoprotein acid (median difference -28.56 mg/dL, 95% CI: -51.57 to -5.07) in burn patients. Decreased serum levels of vitamin A (median difference 1.10 μmol/L, 95% confidence interval [CI]: 0.42-1.66) and vitamin C (median difference 0.82 mg/dL, 95% CI: 0.50-1.04) were also detected. There was no statistical evidence of difference in the serum levels of glutathione peroxidase and thiobarbituric acid reactive substances between burn patients and controls, respectively. Even though there is an inflammatory stress, the obtained data showed that oxidative stress markers are normal 24 to 72 hours after burn injury. The decrease in negative acute phase protein may account for the diminished serum levels of vitamin A, which seems to be related to inflammatory stress. The marked decrease in the serum levels

  13. A Novel Murine Model for Chronic Inflammatory Alveolar Bone loss

    PubMed Central

    Oz, Helieh S; Ebersole, Jeffrey L

    2009-01-01

    Objective Chronic inflammatory bowel disease (IBD) demonstrates some similarities of dysregulated chronic immunoinflammatory lesion of periodontitis. Trinitrobenzene sulfonic acid (TNBS) and dextran sodium sulphate (DSS) administered to rodents have been shown to elicit inflammatory responses that undermine the integrity of the gut epithelium similar to IBD in humans. The objective of this study was to evaluate the ability of these chemicals to elicit periodontal inflammation as a novel model for alveolar bone loss. Methods Mice were treated by oral application of TNBS 2 times/week, or with DSS in the diet over a period of 18 weeks. Alveolar bone loss was assessed on defleshed skull using morphometric measures for area of bone resorption. Results TNBS-treated animals tolerated oral administration with no clinical symptoms and gained weight similar to normal controls. In contrast, DSS exerted a systemic response including shortening of colonic tissue and liver enzyme changes. Both TNBS and DSS caused a localized action on periodontal tissues with alveolar bone loss observed in both maxilla and mandibles with progression in a time dependent manner. Bone loss was detected as early as week 7, with more severe periodontitis increasing over the 18 weeks (p<0.001). Young (7 month) and old (12 month) SCID mice were treated with TNBS for a period of 7 weeks and did not develop significant bone loss. Conclusions These data show that oral administration of TNBS and DSS provoke alveolar bone loss in concert with the autochthonous oral microbiota. PMID:19602109

  14. Peripolesis followed by cytotoxicity in chronic idiopathic inflammatory bowel disease.

    PubMed Central

    Wilders, M M; Drexhage, H A; Kokjé, M; Verspaget, H W; Meuwissen, S G

    1984-01-01

    Antigen presenting veiled cells have recently been described in cell suspensions prepared from the gut wall of patients with chronic idiopathic inflammatory bowel disease (CIBD). The normal gut wall is virtually devoid of these cells. In this report we describe a phenomenon known as peripolesis studied by phase contrast cinematography. This is a process in which lymphocytes are seen to wander around larger target cells. These could be identified ultrastructurally as Ia positive veiled cells. In most cases peripolesis was followed by lysis of the target cell. Peripolesis was recorded in cell suspensions of three out of seven patients with ulcerative colitis and in three out of nine patients with Crohn's disease; furthermore peripolesis was observed in one out of two patients with non-classifiable CIBD. In four cell suspensions showing peripolesis, cell lysis could be recorded and was especially striking in ulcerative colitis. Peripolesis involving veiled cells was previously described in delayed hypersensitivity reactions. This study lends support to the concept that delayed allergic reactivity plays a part in chronic inflammatory bowel disease. The antigens involved are, however, completely unknown. Images Fig. 1 Fig. 2 Fig. 3 PMID:6380839

  15. NF-kappaB Signaling in Chronic Inflammatory Airway Disease

    PubMed Central

    Schuliga, Michael

    2015-01-01

    Asthma and chronic obstructive pulmonary disease (COPD) are obstructive airway disorders which differ in their underlying causes and phenotypes but overlap in patterns of pharmacological treatments. In both asthma and COPD, oxidative stress contributes to airway inflammation by inducing inflammatory gene expression. The redox-sensitive transcription factor, nuclear factor (NF)-kappaB (NF-κB), is an important participant in a broad spectrum of inflammatory networks that regulate cytokine activity in airway pathology. The anti-inflammatory actions of glucocorticoids (GCs), a mainstay treatment for asthma, involve inhibition of NF-κB induced gene transcription. Ligand bound GC receptors (GRs) bind NF-κB to suppress the transcription of NF-κB responsive genes (i.e., transrepression). However, in severe asthma and COPD, the transrepression of NF-κB by GCs is negated as a consequence of post-translational changes to GR and histones involved in chromatin remodeling. Therapeutics which target NF-κB activation, including inhibitors of IκB kinases (IKKs) are potential treatments for asthma and COPD. Furthermore, reversing GR/histone acetylation shows promise as a strategy to treat steroid refractory airway disease by augmenting NF-κB transrepression. This review examines NF-κB signaling in airway inflammation and its potential as target for treatment of asthma and COPD. PMID:26131974

  16. Anti-inflammatory effects of macrolides: applications in chronic rhinosinusitis.

    PubMed

    Harvey, Richard J; Wallwork, Ben D; Lund, Valerie J

    2009-11-01

    The anti-inflammatory effects of macrolides are significant. The clinical impact on diffuse panbronchiolitis (DPB) has improved 10-year survival from 12% to more than 90% for these patients. The immunomodulatory activity of macrolides has been a source of mechanistic research as well as clinical research in non-DPB inflammatory airway disease. Suppression of neutrophilic inflammation of the airways has been demonstrated as the most robust immunomodulatory response from 14- and 15-membered ring macrolides. The inhibition of transcription factors, mainly nuclear factor-kB and activator protein 1, from alterations in intracellular cell signaling drives this mechanism. The suppression of interleukin-8 to a range of endogenous and exogenous challenges characterizes the alterations to cytokine production. The inflammatory mechanisms of chronic rhinosinusitis (CRS) have been a major non-DPB focus. Macrolides have been trialed in more than 14 prospective trials and are the focus of numerous research projects. Evidence for a strong clinical effect in CRS is mounting, but results may be tempered by researchers' inability to characterize the disease process. Eosinophilic dominated CRS is unlikely to respond, based on current research understanding and data from clinical trials. This article discusses the current concepts of macrolides and their application in the management of CRS.

  17. Nutritional and Anti-Inflammatory Interventions in Chronic Heart Failure

    PubMed Central

    Kalantar-Zadeh, Kamyar; Anker, Stefan D; Horwich, Tamara B; Fonarow, Gregg C

    2017-01-01

    Summary Five million individuals with chronic heart failure (CHF) in the United States have poor clinical outcomes including high death rates. Observational studies have indicated a reverse epidemiology of traditional cardiovascular risk factors in CHF; in contrast to trends seen in the general population, obesity and hypercholesterolemia are associated with improved survival. The temporal discordance between the overnutrition (long-term killer) and undernutrition (short-term killer) not only can explain some of the observed paradoxes but also may indicate a role for malnutrition, inflammation and oxidative stress that result in cachexia contributing to poor survival in CHF. Diminished appetite or anorexia may be both a cause and a consequence of this so-called malnutrition-inflammation-cachexia (MIC) or wasting syndrome in CHF. Neurohumoral activation, insulin resistance, cytokine activation and survival selection resultant genetic polymorphisms may also contribute to the prominent inflammatory and oxidative characteristics of this population. In CHF patients with wasting, nutritional strategies may be a promising therapeutic approach in CHF, especially if the provision of additional protein and energy also includes nutrients with anti-inflammatory and anti-oxidant properties. Regardless of the etiology of anorexia, appetite stimulating agents especially with anti-inflammatory properties such as megesterol acetate or pentoxyphylline may be appropriate adjuncts to dietary supplementation. Understanding the factors that modulate the MIC and wasting and their associations with clinical outcomes in CHF may lead to the development of nutritional strategies that alter the pathophysiology of CHF and improve outcomes PMID:18514634

  18. Adipokine CTRP-5 as a Potential Novel Inflammatory Biomarker in Chronic Obstructive Pulmonary Disease

    PubMed Central

    Li, Diandian; Wu, Yanqiu; Tian, Panwen; Zhang, Xue; Wang, Hao; Wang, Tao; Ying, Binwu; Wang, Lanlan; Shen, Yongchun; Wen, Fuqiang

    2015-01-01

    Abstract Local and systemic inflammation often present in chronic obstructive pulmonary disease (COPD). Adipokines are secretory protein mediators by adipose tissue, which have been found to involve in inflammatory responses in many chronic inflammatory diseases. Therefore, we performed this preliminary clinical study to investigate the possible association between 2 adipokines, C1q/tumor necrosis factor-related protein-3 and -5 (CTRP-3 and CTRP-5), with lung function and other markers of inflammation in COPD. Serum CTRP-3 and CTRP-5 levels were measured in 73 COPD patients and 54 health controls, together with lung function and levels of adiponectin, CRP, TNF-α, and MPO in both groups. Pearson's partial correlation was used to analyze the correlations between CTRPs and other serum markers or lung function. Serum CTRP-5 was significantly elevated in COPD patients (0.41 ± 0.35 versus 0.29 ± 0.28 μg/ml, P = 0.01) and correlated inversely with FEV1/FVC ratio in all patients (r = −0.31, P = 0.001). In COPD patients, CTRP-5 was also correlated negatively with FEV1% predicted (r = −0.464, P < 0.001) and had a positive association with CRP levels (r = 0.262, P = 0.04). However, serum CTRP-3 levels were not correlated with measures of lung function or systemic inflammation. In conclusion, circulating CTRP-5 was associated with the severity of airflow obstruction and systemic inflammation in patients with COPD, which suggests that it may be used as a potential novel inflammatory biomarker in COPD. Further studies should be performed to clarify the exact role of CTRP-5 on the pathogenesis and outcomes of COPD. PMID:26356719

  19. EFFECT OF THREE DIFFERENT SIZED FRACTIONS OF OUTDOOR PM ON INFLAMMATORY AND OXIDATIVE MARKERS IN VIVO

    EPA Science Inventory

    EFFECT OF THREE DIFFERENT SIZED FRACTIONS OF OUTDOOR PM ON INFLAMMATORY MARKERS IN VIVO
    C A J Dick', P Singh2, P. Evansky3, S Becker3 and M I Gilmour3.
    'Center For Environmental Medicine and Lung Biology, UNC, Chapel Hill, NC 27599 2NCSU, Raleigh, NC 'Experimental Toxicolog...

  20. Novel inflammatory markers associated with cognitive performance: Singapore Longitudinal Ageing Studies.

    PubMed

    Gao, Qi; Camous, Xavier; Lu, Yan-Xia; Lim, May-Li; Larbi, Anis; Ng, Tze-Pin

    2016-03-01

    We identified and validated several novel inflammatory markers of cognitive performance in community-living older persons. An exploratory study (n = 83) correlated 177 inflammatory markers assayed by Luminex with the Mini-Mental State Examination (MMSE) and identified 8 inflammatory markers for enzyme-linked immunosorbent assay (ELISA) and correlations with MMSE, Montreal Cognitive Assessment (MoCA), and cognitive impairment in the validation study (n = 139). The validation study replicated the significant associations of soluble interleukin-2 receptor alpha chain (sIL-2Rα; p = 0.050), soluble tumor necrosis factor receptor 2 (sTNFR2; p = 0.002) and soluble glycoprotein 130 (sgp130; p = 0.026) with MMSE, and sIL-2Rα (p = 0.019) and sgp130 (p < 0.001) with MoCA. Significant trends of associations of tertiles of sgp130, sIL-2Rα, and sTNFR2 were found with cognitive impairment. Highly elevated estimates of association of high versus low tertiles were obtained for sgp130 (odds ratio [OR] = 4.24, 95% confidence interval [CI] 0.96-18.8), sIL-2Rα (OR = 3.94, 95% CI 0.83-18.7), and sTNFR2 (OR = 7.58, 95% CI 1.19-48.1). sgp130, sTNFR2, and sIL-2Rα are promising inflammatory markers of low cognitive performance for further investigation.

  1. Associated among endocrine, inflammatory, and bone markers, body composition and weight loss induced bone loss

    USDA-ARS?s Scientific Manuscript database

    Weight loss reduces co-¬morbidities of obesity but decreases bone mass. Our aims were to determine whether adequate dairy intake could prevent weight loss related bone loss and to evaluate the contribution of energy-related hormones and inflammatory markers to bone metabolism. Overweight and obese w...

  2. Relation of Smoking Status to a Panel of Inflammatory Markers: The Framingham Offspring

    PubMed Central

    Levitzky, Yamini S.; Guo, Chao-Yu; Rong, Jian; Larson, Martin G.; Walter, Robert E.; Keaney, John F.; Sutherland, Patrice A.; Vasan, Aditi; Lipinska, Izabella; Evans, Jane C.; Benjamin, Emelia J.

    2008-01-01

    Aims We sought to investigate the hypothesis that smoking is accompanied by systemic inflammation. Methods and Results We examined the relation of smoking to 11 systemic inflammatory markers in Framingham Study participants (n=2944, mean age 60 years, 55% women, 12% ethnic minorities) examined from 1998–2001. The cohort was divided into never (n=1149), former (n=1424), and current smokers with last cigarette >6 hours (n=134) or ≤6 hours (n=237) prior to phlebotomy. In multivariable-adjusted models there were significant overall between-smoking group differences (defined as p<0.0045 to account for multiple testing) for every inflammatory marker tested, except for serum CD40 ligand (CD40L), myeloperoxidase (MPO) and tumor necrosis factor receptor-2 (TNFR2). With multivariable-adjustment, pair-wise comparisons with never smokers revealed that former smokers had significantly lower concentrations of plasma CD40L (p<0.0001) and higher concentrations of C-reactive protein (p=0.002). Conclusions As opposed to never smokers, those with acute cigarette smoke exposure (≤6 hours) had significantly higher concentrations of all markers (p<0.0001) except serum CD40L, MPO, and TNFR2; plasma CD40L were significantly lower. Compared with never smokers, cigarette smokers have significantly elevated concentrations of most circulating inflammatory markers, consistent with the hypothesis that smoking is associated with a systemic inflammatory state. PMID:18289552

  3. Relation of smoking status to a panel of inflammatory markers: the framingham offspring.

    PubMed

    Levitzky, Yamini S; Guo, Chao-Yu; Rong, Jian; Larson, Martin G; Walter, Robert E; Keaney, John F; Sutherland, Patrice A; Vasan, Aditi; Lipinska, Izabella; Evans, Jane C; Benjamin, Emelia J

    2008-11-01

    We sought to investigate the hypothesis that smoking is accompanied by systemic inflammation. We examined the relation of smoking to 11 systemic inflammatory markers in Framingham Study participants (n=2944, mean age 60 years, 55% women, 12% ethnic minorities) examined from 1998-2001. The cohort was divided into never (n=1149), former (n=1424), and current smokers with last cigarette >6h (n=134) or < or =6h (n=237) prior to phlebotomy. In multivariable-adjusted models there were significant overall between-smoking group differences (defined as p<0.0045 to account for multiple testing) for every inflammatory marker tested, except for serum CD40 ligand (CD40L), myeloperoxidase (MPO) and tumor necrosis factor receptor-2 (TNFR2). With multivariable-adjustment, pair-wise comparisons with never smokers revealed that former smokers had significantly lower concentrations of plasma CD40L (p<0.0001) and higher concentrations of (CRP) C-reactive protein (p=0.002). As opposed to never smokers, those with acute cigarette smoke exposure (< or =6h) had significantly higher concentrations of all markers (p<0.0001) except serum CD40L, MPO, and TNFR2; plasma CD40L were significantly lower. Compared with never smokers, cigarette smokers have significantly elevated concentrations of most circulating inflammatory markers, consistent with the hypothesis that smoking is associated with a systemic inflammatory state.

  4. Role of Pro-Inflammatory Cytokines and Biochemical Markers in the Pathogenesis of Type 1 Diabetes: Correlation with Age and Glycemic Condition in Diabetic Human Subjects.

    PubMed

    Fatima, Naureen; Faisal, Syed Mohd; Zubair, Swaleha; Ajmal, Mohd; Siddiqui, Sheelu Shafiq; Moin, Shagufta; Owais, Mohammad

    2016-01-01

    Type 1 diabetes mellitus is a chronic inflammatory disease involving insulin producing β-cells destroyed by the conjoined action of auto reactive T-cells, inflammatory cytokines and monocytic cells. The aim of this study was to elucidate the status of pro-inflammatory cytokines and biochemical markers and possible correlation of these factors towards outcome of the disease. The study was carried out on 29 T1D subjects and 20 healthy subjects. Plasma levels of oxidative stress markers, enzymatic and non-enzymatic antioxidants were estimated employing biochemical assays. The levels of pro-inflammatory cytokines such as by IL-1β & IL-17 in the serum were determined by ELISA, while the expression of TNF-α, IL-23 & IFN-γ was ascertained by qRT-PCR. The onset of T1D disease was accompanied with elevation in levels of Plasma malondialdehyde, protein carbonyl content and nitric oxide while plasma vitamin C, reduced glutathione and erythrocyte sulfhydryl groups were found to be significantly decreased in T1D patients as compared to healthy control subjects. Activity of antioxidant enzymes, superoxide dismutase, catalase, glutathione reductase and glutathione-s-transferase showed a significant suppression in the erythrocytes of T1D patients as compared to healthy subjects. Nevertheless, the levels of pro-inflammatory cytokines IL-1β and IL-17A were significantly augmented (***p≤.001) on one hand, while expression of T cell based cytokines IFN-γ, TNF-α and IL-23 was also up-regulated (*p≤.05) as compared to healthy human subjects. The level of pro-inflammatory cytokines and specific biochemical markers in the serum of the patient can be exploited as potential markers for type 1 diabetes pathogenesis. The study suggests that level of inflammatory markers is up-regulated in T1D patients in an age dependent manner.

  5. Serum Inflammatory Mediators as Markers of Human Lyme Disease Activity

    PubMed Central

    Soloski, Mark J.; Crowder, Lauren A.; Lahey, Lauren J.; Wagner, Catriona A.

    2014-01-01

    Chemokines and cytokines are key signaling molecules that orchestrate the trafficking of immune cells, direct them to sites of tissue injury and inflammation and modulate their states of activation and effector cell function. We have measured, using a multiplex-based approach, the levels of 58 immune mediators and 7 acute phase markers in sera derived from of a cohort of patients diagnosed with acute Lyme disease and matched controls. This analysis identified a cytokine signature associated with the early stages of infection and allowed us to identify two subsets (mediator-high and mediator-low) of acute Lyme patients with distinct cytokine signatures that also differed significantly (p<0.0005) in symptom presentation. In particular, the T cell chemokines CXCL9 (MIG), CXCL10 (IP-10) and CCL19 (MIP3B) were coordinately increased in the mediator-high group and levels of these chemokines could be associated with seroconversion status and elevated liver function tests (p = 0.027 and p = 0.021 respectively). There was also upregulation of acute phase proteins including CRP and serum amyloid A. Consistent with the role of CXCL9/CXCL10 in attracting immune cells to the site of infection, CXCR3+ CD4 T cells are reduced in the blood of early acute Lyme disease (p = 0.01) and the decrease correlates with chemokine levels (p = 0.0375). The levels of CXCL9/10 did not relate to the size or number of skin lesions but elevated levels of serum CXCL9/CXCL10 were associated with elevated liver enzymes levels. Collectively these results indicate that the levels of serum chemokines and the levels of expression of their respective chemokine receptors on T cell subsets may prove to be informative biomarkers for Lyme disease and related to specific disease manifestations. PMID:24740099

  6. Inulin and oligofructose in chronic inflammatory bowel disease.

    PubMed

    Leenen, Celine H M; Dieleman, Levinus A

    2007-11-01

    Crohn's disease and ulcerative colitis, also called chronic inflammatory bowel diseases (IBD), affect up to 500 per 100,000 persons in the Western world. Recent studies in the etiology of IBD suggest that these diseases are caused by a combination of genetic, environmental, and immunological factors. Results from humans and especially animal models of colitis reported by our group and others have indicated that these diseases result from a lack of tolerance to resident intestinal bacteria in genetically susceptible hosts. Probiotic bacteria have health-promoting effects for the host when ingested and have also shown efficacy in ulcerative colitis and refractory pouchitis. In light of the efficacy of providing probiotic bacteria to patients with IBD, there has been interest in the prophylactic and therapeutic potential of inulin, oligofructose, and other prebiotics for patients with or at risk of IBD. Prebiotics are nondigestible dietary oligosaccharides that affect the host by selectively stimulating growth, activity, or both of selective intestinal (probiotic) bacteria. Prebiotics are easy to administer and, in contrast to probiotic therapy, do not require administration of large amounts of (live) bacteria and are therefore easier to administer. Studies using prebiotics, especially beta-fructan oligosaccharides, for the treatment of chronic intestinal inflammation have shown benefit in animal models of colitis. Studies using these prebiotics alone or in combination with probiotics are emerging and have shown promise. These dietary therapies could lead to novel treatments for these chronic debilitating diseases.

  7. Associations of Amylin with Inflammatory Markers and Metabolic Syndrome in Apparently Healthy Chinese

    PubMed Central

    Li, Zongmeng; Mou, Haiwei; Yu, Zhijie; Li, Huaixing; Jiang, Peizhen; Yu, Danxia; Wu, Hongyu; Ye, Xingwang; Lin, Xu; Le, Yingying

    2011-01-01

    Background Cellular and animal studies implicate multiple roles of amylin in regulating insulin action, glucose and lipid metabolisms. However, the role of amylin in obesity related metabolic disorders has not been thoroughly investigated in humans. Therefore, we aimed to evaluate the distribution of circulating amylin and its association with metabolic syndrome (MetS) and explore if this association is influenced by obesity, inflammatory markers or insulin resistance in apparently healthy Chinese. Methods A population-based sample of 1,011 Chinese men and women aged 35–54 years was employed to measure plasma amylin, inflammatory markers (C-reactive protein [CRP] and interleukin-6 [IL-6]), insulin, glucose and lipid profiles. MetS was defined according to the updated National Cholesterol Education Program Adult Treatment Panel III criteria for Asian-Americans. Results Plasma amylin concentrations were higher in overweight/obese participants than normal-weight counterparts (P<0.001) without sex difference. Circulating amylin was positively associated with CRP, IL-6, BMI, waist circumference, blood pressure, fasting glucose, insulin, amylin/insulin ratio, HOMA-IR, LDL cholesterol and triglycerides, while negatively associated with HDL cholesterol (all P<0.001). After multiple adjustments, the risk of MetS was significantly higher (odds ratio 3.71; 95% confidence interval: 2.53 to 5.46) comparing the highest with the lowest amylin quartile. The association remained significant even further controlling for BMI, inflammatory markers, insulin or HOMA-IR. Conclusions Our study suggests that amylin is strongly associated with inflammatory markers and MetS. The amylin-MetS association is independent of established risk factors of MetS, including obesity, inflammatory markers and insulin resistance. The causal role of hyperamylinemia in the development of MetS needs to be confirmed prospectively. PMID:21935471

  8. Relationship between Inflammatory Markers, Endothelial Activation Markers, and Carotid Intima-Media Thickness in HIV-Infected Patients Receiving Antiretroviral Therapy

    PubMed Central

    Ross, Allison C.; Rizk, Nesrine; O'Riordan, Mary Ann; Dogra, Vikram; El-Bejjani, Dalia; Storer, Norma; Harrill, Danielle; Tungsiripat, Marisa; Adell, Jerome; McComsey, Grace A.

    2014-01-01

    Background Human immunodeficiency virus (HIV)–infected patients are at increased risk of cardiovascular disease, which may be related to chronic inflammation and endothelial dysfunction despite virological control with antiretroviral therapy. The relationship between carotid intima-media thickness (IMT), a surrogate marker for cardiovascular disease, proinflammatory cytokines, and endothelial activation markers has not been fully explored in HIV-infected patients who are receiving antiretroviral therapy. Methods We conducted a prospective, cross-sectional, observational study of treated HIV-infected patients and healthy control subjects to evaluate the relationship between carotid IMT, proinflammatory cytokines, endothelial activation biomarkers, and metabolic parameters in treated HIV-infected patients, compared with healthy control subjects. Results We enrolled 73 HIV-infected patients and 21 control subjects. Common carotid artery and internal carotid artery IMT measurements, as well as tumor necrosis factor–α, high-sensitivity C-reactive protein, inter-leukin-6, myeloperoxidase, and soluble vascular cell adhesion molecule-1 levels were higher in the HIV-infected group. High-sensitivity C-reactive protein was the only biomarker that was positively correlated with carotid IMT in both groups. In the HIV-infected group, soluble vascular cell adhesion molecule–1 was positively correlated with all inflammatory cytokine levels. In multiple regression analysis, soluble vascular cell adhesion molecule–1, myeloperoxidase, and tumor necrosis factor–α levels were all associated with internal carotid artery IMT in the HIV-infected group, whereas age was associated with both common carotid artery and internal carotid artery IMT. Conclusions Enhanced endothelial activation, inflammation, and increased carotid IMT occur in HIV-infected patients despite antiretroviral therapy. Inflammatory markers are associated with endothelial activation, and both are associated

  9. Serum Golgi Protein 73 (GP73) is a Diagnostic and Prognostic Marker of Chronic HBV Liver Disease

    PubMed Central

    Xu, Zhengju; Liu, Liguan; Pan, Xingnan; Wei, Kaipeng; Wei, Meijuan; Liu, Lifei; Yang, Huanwen; Liu, Qian

    2015-01-01

    Abstract Alanine aminotransferase (ALT) is the most commonly used marker of liver injury, but normal ALT levels are seen in a proportion of chronic hepatitis B virus (HBV)-infected patients with severe liver injury. Golgi protein 73 (GP73) is a promising alternative marker of liver injury. This study assessed the relation between GP73 levels and liver disease severity, monitored the kinetic changes in GP73 levels in chronic HBV patients receiving entecavir (ETV) therapy, and investigated the potential diagnostic and prognostic values of serum GP73 as a new liver injury biomarker in chronic HBV infections. This study enrolled 1150 patients with chronic HBV infections, 200 of whom were retrospectively enrolled in this study after receiving 1 year of ETV treatment. GP73 expression in liver tissue was detected by immunohistochemistry. GP73 levels in single or serial serum samples were measured by enzyme-linked immunosorbent assay. Immunohistochemical analysis indicated that GP73 protein expression in the liver increased progressively with pathologic progression from nonexistent or mild hepatitis to severe hepatitis and cirrhosis during chronic HBV infection. Serum GP73 levels were positively correlated with the disease severity of chronic HBV infections (r = 0.58, P < 0.001). In patients with normal ALT levels, serum GP73 concentrations were significantly higher in patients with prominent hepatic inflammatory injury and fibrosis than in patients without hepatic inflammatory injury or fibrosis. Serum GP73 concentrations and GP73 protein expression were decreased in the liver tissues of patients whose ALT levels normalized after 1 year of ETV antiviral therapy. Changes in serum GP73 levels were closely associated with changes in liver injury severity, and, therefore, GP73 may be an effective new liver inflammatory injury biomarker, and could be useful for monitoring the prognosis of chronic HBV infectious patients with normal ALT levels. PMID:25816035

  10. [Association between inflammatory markers and microbial translocation in patients with human immunodeficiency virus infection taking antiretroviral treatment].

    PubMed

    Reus Bañuls, Sergio; Portilla Sogorb, Joaquín; Sanchez-Paya, José; Boix Martínez, Vicente; Giner Oncina, Livia; Frances, Rubén; Such, José; Merino Lucas, Esperanza; Gimeno Gascón, Adelina

    2014-01-21

    Inflammatory biomarkers are increased in patients with human immunodeficiency virus (HIV) infection. Antiretroviral treatment (ART) improves some parameters but do not normalize them. The aim of this study is to determine those factors (including microbial translocation) associated with higher inflammation in HIV treated patients. Transversal observational study. HIV patients receiving ART with an HIV viral load (VL)<400 copies/mL. Selection of patients: consecutively between November 2011 and January 2012. Main variable: plasma levels of interleukin 6 (IL-6) and tumour necrosis factor α (TNF-α). Main explanatory variable: microbial translocation markers (16S ribosomal DNA and sCD14). Patients with IL-6 or TNF-α levels above percentile 75 (group 1) were compared with the rest of patients (group 2). Odds ratio (OR) were determined. Eighty-one patients were included (73% male, median age 45 years, 48% stage C). Twenty-six percent had chronic hepatitis C. Median CD4 cell was 493/mm(3) and 30% had detectable HIV VL. 16S ribosomal DNA was detected in 21% of patients. Factors associated with the higher levels of inflammatory markers were 16S ribosomal DNA (OR 77, P<.0001), sCD14 levels (P<.0001) and history of cardiovascular disease (OR 15, P<.01). In multivariate analysis, associations remained for 16S ribosomal DNA (OR 62, P<.0001) and previous cardiovascular disease (OR 25, P<.01). In patients with HIV infection receiving treatment, the higher levels of inflammatory markers are associated with microbial translocation and past cardiovascular events. Copyright © 2013 Elsevier España, S.L. All rights reserved.

  11. Faecal alpha-1-antitrypsin and excretion of 111indium granulocytes in assessment of disease activity in chronic inflammatory bowel diseases.

    PubMed Central

    Fischbach, W; Becker, W; Mössner, J; Koch, W; Reiners, C

    1987-01-01

    Intestinal protein loss in chronic inflammatory bowel diseases may be easily determined by measurement of alpha-1-antitrypsin (alpha 1-AT) stool concentration and alpha 1-AT clearance. Both parameters were significantly raised in 36 and 34 patients respectively with chronic inflammatory bowel diseases, compared with eight patients with non-inflammatory bowel diseases, or 19 healthy volunteers. There was wide range of overlap between active and inactive inflammatory disease. Contrary to serum alpha 1-AT, faecal excretion and clearance of alpha 1-AT did not correlate with ESR, serum-albumin, orosomucoid, and two indices of disease activity. A comparison of alpha 1-AT faecal excretion and clearance with the faecal excretion of 111In labelled granulocytes in 27 patients with chronic inflammatory bowel diseases, showed no correlation between the intestinal protein loss and this highly specific marker of intestinal inflammation. Enteric protein loss expressed by faecal excretion and clearance of alpha 1-AT does not depend on mucosal inflammation only, but may be influenced by other factors. PMID:3495470

  12. Genetic Effects on Postprandial Variations of Inflammatory Markers in Healthy Individuals

    PubMed Central

    Cheng, Yu-Ching; Kao, Wen-Hong L.; Mitchell, Braxton D.; Sharrett, A. Richey; Ryan, Kathleen A.; Vogel, Robert A.; Shuldiner, Alan R.; Pollin, Toni I.

    2011-01-01

    Circulating levels of inflammatory markers predict the risk of cardiovascular disease (CVD), mediated perhaps in part by dietary fat intake, through mechanisms only partially understood. To evaluate post-fat load changes in inflammatory markers and genetic influences on these changes, we administered a standardized high-fat meal to 838 related Amish subjects as part of the Heredity and Phenotype Intervention (HAPI) Heart Study and measured a panel of inflammatory markers, including C-reactive protein (CRP), interleukin-1 β (IL-1β), matrix metalloproteinase-1 and -9 (MMP-1 and MMP-9), and white blood cell (WBC) count, before and 4 hours post-fat challenge (CRP pre-challenge only). Heritabilities (h2 ± SD) of basal inflammatory levels ranged from 16 ± 8% for MMP-9 (P = 0.02) to 90 ± 7% for MMP-1 (P < 0.0001). Post-fat load, circulating levels of WBC, MMP-1 and MMP-9 increased by 16%, 32% and 43% (all P < 0.0001), with no significant changes in IL-1β. Postprandial changes over the 4-hour period were modestly heritable for WBC (age- and sex-adjusted h2 = 14 ± 9%, P = 0.04), but the larger MMP-1 and MMP-9 changes appeared to be independent of additive genetic effects. These results reveal that a high fat meal induces a considerable inflammatory response. Genetic factors appear to play a significant role influencing basal inflammatory levels but to have minimal influence on post-fat intake inflammatory changes. PMID:19910936

  13. Chronic recurrent multifocal osteomyelitis associated with chronic inflammatory bowel disease in children.

    PubMed

    Bousvaros, A; Marcon, M; Treem, W; Waters, P; Issenman, R; Couper, R; Burnell, R; Rosenberg, A; Rabinovich, E; Kirschner, B S

    1999-12-01

    Chronic recurrent multifocal osteomyelitis (CRMO) is a rare disease of children characterized by aseptic inflammation of the long bones and clavicles. No infectious etiology has been identified, and CRMO has been associated with a number of autoimmune diseases (including Wegener's granulomatosis and psoriasis). The relationship between CRMO and inflammatory bowel disease is poorly described. Through an internet bulletin board subscribed to by 500 pediatric gastroenterologists, we identified six inflammatory bowel disease patients (two with ulcerative colitis, four with Crohn's colitis) with confirmed CRMO. In all cases, onset of the bony lesions preceded the onset of bowel symptoms by as much as five years. Immunosuppressive therapy for the bowel disease generally resulted in improvement of the bone inflammation. Chronic recurrent multifocal osteomyelitis should be considered in any inflammatory bowel disease patient with unexplained bone pain or areas of uptake on bone scan. CRMO may be a rare extraintestinal manifestation of inflammatory bowel disease; alternatively, certain individuals may be genetically predisposed to the development of both diseases.

  14. Neutrophil anti-neutrophil cytoplasmic autoantibody proteins: bactericidal increasing protein, lactoferrin, cathepsin, and elastase as serological markers of inflammatory bowel and other diseases

    PubMed Central

    Kyriakidi, Kallirroi S.; Tsianos, Vasileios E.; Karvounis, Evaggelos; Christodoulou, Dimitrios K.; Katsanos, Konstantinos H.; Tsianos, Epameinondas V.

    2016-01-01

    Inflammatory bowel disease (IBD) is a chronic inflammatory disorder of the gastrointestinal tract comprising Crohn’s disease and ulcerative colitis. Although the pathogenesis of the disease is not clearly defined yet, environmental, genetic and other factors contribute to the onset of the disease. Apart from the clinical and histopathological findings, several serological biomarkers are also employed to detect IBD. One of the most thoroughly studied biomarker is anti-neutrophil cytoplasmic autoantibody (ANCA). We herein provide an overview of the current knowledge on the use of ANCA and certain ANCA proteins, such as bactericidal increasing protein, lactoferrin, cathepsin G and elastase, as serological markers for IBD and other diseases. PMID:27366026

  15. [Treatment's initiation in chronic inflammatory demyelinating polyradiculopathy (CIDP)].

    PubMed

    Uzenot, D; Azulay, J-P; Pouget, J

    2007-09-01

    Treatment's initiation in chronic inflammatory demyelinating polyradiculopathy (CIDP) remains a difficult medical decision. Only plasma exchanges, intravenous immunoglobulins (IVIg) and corticosteroids are proven effective treatments. Immunosuppressors are actually not first-line treatments in CIDP. Particular CIDP forms are associated with different response to treatments: pure motor CIDP should be treated by IVIg, and corticosteroids should only carefully be used in Lewis-Sumner syndrome. Otherwise, IVIg are first-line treatment in diabetic patients. Patients must be informed of side's effects and expected clinical effects. Early treatment was actually not proved to prevent axonal damages in CIDP patients, and waiting seems to be the best therapeutic option in poorly symptomatic patients. Recently, clinical guidelines were proposed to help clinician in this treatment choice, but there is no consensus about the best dose, duration or administration way to CIDP treatments. Further studies should be performed to clarify these points and to determine immunosuppressor agents place in treatment strategy.

  16. Chronic idiopathic inflammatory bowel diseases: the histology report.

    PubMed

    Cornaggia, Matteo; Leutner, Monica; Mescoli, Claudia; Sturniolo, Giacomo Carlo; Gullotta, Renzo

    2011-03-01

    The incidence of chronic idiopathic inflammatory bowel diseases (IBD) is growing in western countries, making their histological diagnosis an everyday task for all pathologists. Reviews from the literature strongly suggest that such diagnosis cannot be performed on the histological ground alone but requires a clinical-pathological approach. Moreover, bewildering variations can be observed in the terminology employed to report either individual lesions or diagnostic categories. The aim of the present paper is to suggest a practical diagnostic algorithm summarizing the main data from the literature. Particular emphasis has been placed on minimum clinical information required and the accurate definition of individual lesions. Diagnostic categories to employ and to avoid in daily practice have furthermore been stressed.

  17. Fibrillary glomerulonephritis combined with chronic inflammatory demyelinating polyneuropathy

    PubMed Central

    Sung, Woo Kyung; Jeong, Jin Uk; Bang, Ki Tae; Shin, Jong Ho; Yoo, Ji Hyung; Kim, Nak Min; Park, Jun Hyung; Kim, Joo Heon

    2015-01-01

    A 58-yr-old man presented with leg edema and subacute weakness of his bilateral lower extremities. Urinary and serum immunoelectrophoresis revealed the presence of lambda-type Bence Jones proteins. He was ultimately diagnosed with monoclonal gammopathy of undetermined significance (MGUS). A renal biopsy specimen showed fibrillary glomerulonephritis (FGN), which was randomly arranged as 12–20 m nonbranching fibrils in the basement membranes. Immunofluorescence studies were negative for immunoglobulin (Ig)G, IgM, IgA, C3, and kappa light chains in the capillary walls and mesangial areas. A Congo red stain for amyloid was negative. Electromyography and nerve conduction velocity examinations results were compatible with the presence of demyelinating polyneuropathy. This case showed a rare combination of FGN, without Ig deposition, and MGUS combined with chronic inflammatory demyelinating polyneuropathy (CIDP). PMID:26484033

  18. [Subcutaneous immunoglobulin. Treatment in chronic inflammatory demyelinating polyradiculo-neuropathy].

    PubMed

    Nogués, Martín A; Varela, Francisco J; Seminario, Gisela; Insúa, María C; Bezrodnik, Liliana

    2016-01-01

    Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is an acquired disease that may affect nerve roots and peripheral nerves. Despite its low incidence, diagnosis is particularly important because there are different effective treatments. Human immunoglobulin is one of the mainstays of the treatment. Although there are few studies up to date, subcutaneous immunoglobulin (IgSC) has been proposed as an alternative to intravenous administration with similar efficacy. We present three cases with definite CIDP, classified according to the European Federation of Neurological Societies / Peripheral Nerve, Society (EFNS /PNS) criteria in which was used SCIgG as a treatment after success with the intravenous route. The Overall Neuropathy Limitations Scale (ONLS) was used to estimate the changes in the muscular strength before and after treatment.

  19. Standard and escalating treatment of chronic inflammatory demyelinating polyradiculoneuropathy

    PubMed Central

    Yoon, Min-Suk; Chan, Andrew; Gold, Ralf

    2011-01-01

    Chronic inflammatory demyelinating polyneuropathy (CIDP) is an acquired, immune-mediated polyradiculoneuritis that is progressive or relapsing over a period of at least 8 weeks. Although the exact pathogenesis is unclear, it is thought to be mediated by both cellular and humoral immune reactions directed against the peripheral nerve myelin or axon. CIDP also involves spinal nerve roots. Early medical treatment of CIDP is important to prevent axonal loss. Only three treatment regimens for CIDP have demonstrated benefit in randomized, controlled studies: corticosteroids, plasma exchange, and intravenous immunoglobulins (IVIg). Approximately 25% of patients respond inadequately to corticosteroids, plasma exchange or IVIg. Large placebo-controlled trials with alternative immunosuppressive compounds, e.g. mycophenolate mofetil, cyclosporine, cyclophosphamide, or monoclonal antibodies, are lacking. PMID:21694819

  20. Intractable chronic inflammatory demyelinating polyneuropathy treated successfully with ciclosporin

    PubMed Central

    Odaka, M; Tatsumoto, M; Susuki, K; Hirata, K; Yuki, N

    2005-01-01

    Background: Chronic inflammatory demyelinating polyneuropathy (CIDP) is a heterogeneous disorder and both clinical course and response to treatment vary widely. Because of the propensity for relapse, CIDP requires maintenance therapy after the initial response to treatment. There is no consensus regarding this in the published literature. Present report: A patient with CIDP was treated with oral prednisolone and cyclophosphamide pulse therapy but required repeated plasma exchange and intravenous immunoglobulin (IVIg). Treatment with ciclosporin freed the patient from repeated IVIg administration. Therapeutic responses in 14 subsequent cases including three patients who showed improvement with ciclosporin are also presented along with an algorithm of the authors' suggested protocol for treatment. Conclusion: Ciclosporin should be considered for patients with intractable CIDP who require repeated IVIg. PMID:16024890

  1. Acute and chronic over-exertion: do depressed immune responses provide useful markers?

    PubMed

    Shephard, R J; Shek, P N

    1998-04-01

    There are ethical objections to inducing cumulative muscle damage and associated decrements of performance deliberately in a healthy athlete. Available data on acute and chronic over-exertion thus include the changes of immune response observed following a single bout of exhausting exercise, sequential observations made on top-level competitors as they approach peak training periods, and longitudinal laboratory studies of heavy (but not necessarily damaging) bouts of training. In all three of these situations, subclinical muscle damage initiates an acute inflammatory response, with a resulting deterioration in physical performance. Although much smaller in degree and shorter in duration, the associated changes in immune function are similar to those seen in sepsis. There have been major advances in immunological technique over the past decade, and significant changes in a number of elements of the immune response can be identified in athletes during periods of heavy training. The most promising immunological marker of excessive training seems a decrease in salivary IgA concentration. However, no single change occurs with sufficient consistency to identify the individual competitor who is at risk of overtraining. Mechanisms can be conceived that convert a sequence of excessive training bouts into an acute and then a chronic inflammatory process, but the syndrome of overtraining has a complex overlay of biological and psychological influences. It remains more easily detected by decreases in physical performance and alterations in mood state than by changes in immune function.

  2. Night shift work and inflammatory markers in male workers aged 20-39 in a display manufacturing company.

    PubMed

    Kim, Seong-Woo; Jang, Eun-Chul; Kwon, Soon-Chan; Han, Wook; Kang, Min-Sung; Nam, Young-Hyeon; Lee, Yong-Jin

    2016-01-01

    ,557 ± 124 and 6,498 ± 144 cells/μL, respectively (p < 0.001). A significant association between shift work and increases in inflammatory markers was confirmed. Because chronic low-grade inflammation plays an important role in the development of cardiovascular diseases, regular follow-up of inflammatory markers as a marker of cardiovascular diseases in shift workers may serve as an early indicator in predicting the effects of shift work on health.

  3. Inflammatory endotypes of chronic rhinosinusitis based on cluster analysis of biomarkers.

    PubMed

    Tomassen, Peter; Vandeplas, Griet; Van Zele, Thibaut; Cardell, Lars-Olaf; Arebro, Julia; Olze, Heidi; Förster-Ruhrmann, Ulrike; Kowalski, Marek L; Olszewska-Ziąber, Agnieszka; Holtappels, Gabriele; De Ruyck, Natalie; Wang, Xiangdong; Van Drunen, Cornelis; Mullol, Joaquim; Hellings, Peter; Hox, Valerie; Toskala, Elina; Scadding, Glenis; Lund, Valerie; Zhang, Luo; Fokkens, Wytske; Bachert, Claus

    2016-05-01

    Current phenotyping of chronic rhinosinusitis (CRS) into chronic rhinosinusitis with nasal polyps (CRSwNP) and chronic rhinosinusitis without nasal polyps (CRSsNP) might not adequately reflect the pathophysiologic diversity within patients with CRS. We sought to identify inflammatory endotypes of CRS. Therefore we aimed to cluster patients with CRS based solely on immune markers in a phenotype-free approach. Secondarily, we aimed to match clusters to phenotypes. In this multicenter case-control study patients with CRS and control subjects underwent surgery, and tissue was analyzed for IL-5, IFN-γ, IL-17A, TNF-α, IL-22, IL-1β, IL-6, IL-8, eosinophilic cationic protein, myeloperoxidase, TGF-β1, IgE, Staphylococcus aureus enterotoxin-specific IgE, and albumin. We used partition-based clustering. Clustering of 173 cases resulted in 10 clusters, of which 4 clusters with low or undetectable IL-5, eosinophilic cationic protein, IgE, and albumin concentrations, and 6 clusters with high concentrations of those markers. The group of IL-5-negative clusters, 3 clusters clinically resembled a predominant chronic rhinosinusitis without nasal polyps (CRSsNP) phenotype without increased asthma prevalence, and 1 cluster had a TH17 profile and had mixed CRSsNP/CRSwNP. The IL-5-positive clusters were divided into a group with moderate IL-5 concentrations, a mixed CRSsNP/CRSwNP and increased asthma phenotype, and a group with high IL-5 levels, an almost exclusive nasal polyp phenotype with strongly increased asthma prevalence. In the latter group, 2 clusters demonstrated the highest concentrations of IgE and asthma prevalence, with all samples expressing Staphylococcus aureus enterotoxin-specific IgE. Distinct CRS clusters with diverse inflammatory mechanisms largely correlated with phenotypes and further differentiated them and provided a more accurate description of the inflammatory mechanisms involved than phenotype information only. Copyright © 2016 American Academy of

  4. Inflammatory neuropathies: pathology, molecular markers and targets for specific therapeutic intervention.

    PubMed

    Ubogu, Eroboghene E

    2015-10-01

    Inflammatory neuropathies encompass groups of heterogeneous disorders characterized by pathogenic immune-mediated hematogenous leukocyte infiltration of peripheral nerves, nerve roots or both, with resultant demyelination or axonal degeneration or both. Inflammatory neuropathies may be divided into three major disease categories: Guillain-Barré syndrome (particularly the acute inflammatory demyelinating polyradiculoneuropathy variant), chronic inflammatory demyelinating polyradiculoneuropathy and nonsystemic vasculitic neuropathy (or peripheral nerve vasculitis). Despite major advances in molecular biology, pathology and genetics, the pathogenesis of these disorders remains elusive. There is insufficient knowledge on the mechanisms of hematogenous leukocyte trafficking into the peripheral nervous system to guide the development of specific molecular therapies for immune-mediated inflammatory neuropathies compared to disorders such as psoriasis, inflammatory bowel disease, rheumatoid arthritis or multiple sclerosis. The recent isolation and characterization of human endoneurial endothelial cells that form the blood-nerve barrier provides an opportunity to elucidate leukocyte-endothelial cell interactions critical to the pathogenesis of inflammatory neuropathies at the interface between the systemic circulation and peripheral nerve endoneurium. This review discusses our current knowledge of the classic pathological features of inflammatory neuropathies, attempts at molecular classification and genetic determinants, the utilization of in vitro and in vivo animal models to determine pathogenic mechanisms at the interface between the systemic circulation and the peripheral nervous system relevant to these disorders and prospects for future potential molecular pathology biomarkers and targets for specific therapeutic intervention.

  5. Inflammatory Neuropathies: Pathology, molecular markers and targets for specific therapeutic intervention

    PubMed Central

    Ubogu, Eroboghene E.

    2015-01-01

    Inflammatory neuropathies encompass groups of heterogeneous disorders characterized by pathogenic immune-mediated hematogenous leukocyte infiltration of peripheral nerves, nerve roots or both, with resultant demyelination or axonal degeneration or both. Inflammatory neuropathies may be divided into three major disease categories: Guillain-Barré syndrome (particularly the acute inflammatory demyelinating polyradiculoneuropathy variant), Chronic inflammatory demyelinating polyradiculoneuropathy and nonsystemic vasculitic neuropathy (or peripheral nerve vasculitis). Despite major advances in molecular biology, pathology and genetics, the pathogenesis of these disorders remains elusive. There is insufficient knowledge on the mechanisms of hematogenous leukocyte trafficking into the peripheral nervous system to guide the development of specific molecular therapies for immune-mediated inflammatory neuropathies compared to disorders such as psoriasis, inflammatory bowel disease, rheumatoid arthritis or multiple sclerosis. The recent isolation and characterization of human endoneurial endothelial cells that form the blood-nerve barrier provides an opportunity to elucidate leukocyte-endothelial cell interactions critical to the pathogenesis of inflammatory neuropathies at the interface between the systemic circulation and peripheral nerve endoneurium. This review discusses our current knowledge of the classic pathological features of inflammatory neuropathies, attempts at molecular classification and genetic determinants, the utilization of in vitro and in vivo animal models to determine pathogenic mechanisms at the interface between the systemic circulation and the peripheral nervous system relevant to these disorders and prospects for future potential molecular pathology biomarkers and targets for specific therapeutic intervention. PMID:26264608

  6. Chronic inflammation in FMF: markers, risk factors, outcomes and therapy.

    PubMed

    Ben-Zvi, Ilan; Livneh, Avi

    2011-02-01

    Familial Mediterranean fever (FMF) is the most common of the hereditary periodic fever syndromes. Although the typical clinical course of FMF is characterized by bouts of painful inflammation, this presentation represents only the tip of the iceberg. In many patients inflammation can persist in attack-free periods, as shown by high levels of acute-phase proteins, cytokines and inflammation-induced proteins. This subclinical inflammation puts patients at risk of developing complications such as anemia, splenomegaly, decreased bone mineral density, heart disease and life-threatening amyloid A amyloidosis, among others. In this article, we review the published data on markers and other factors involved in the persistence of inflammation in patients with FMF during attack-free periods, examine the risk factors for the development of this subclinical inflammation, summarize the complications of chronic inflammation in FMF and propose a new strategy for treatment, based on these data.

  7. Prediction of iron deficiency in chronic inflammatory rheumatic disease anaemia.

    PubMed

    Baumann Kurer, S; Seifert, B; Michel, B; Ruegg, R; Fehr, J

    1995-12-01

    We prospectively studied 45 anaemic patients (37 women, 8 men) with chronic inflammatory rheumatic diseases. The combination of serum ferritin and CRP (as well as ESR) in its predictive capacity for bone marrow iron stores was examined. The relationship between other iron-related measurements (transferrin, transferrin saturation, soluble transferrin receptor, erythrocyte porphyrins and percentage of hypochromic/microcytic erythrocytes) and bone marrow iron stores was also investigated. Stainable bone marrow iron was taken as the most suitable standard to separate iron-deficient from iron-replete patients. 14 patients (31%) were lacking bone marrow iron. Regression analysis showed a good correlation between ferritin and bone marrow iron (adjusted R2 = 0.721, P < 0.0001). The combination of ferritin and CRP (ESR) did not improve the predictive power for bone marrow iron (adjusted R2 = 0.715) in this cohort of patients with low systemic inflammatory activity. With respect to the bone marrow iron content the best predictive cut-off value of ferritin was 30 micrograms/l (86% sensitivity, 90% specificity). The other iron-related parameters both individually and when combined were less powerful in predicting bone marrow iron than ferritin alone. Only zinc bound erythrocyte protoporphyrin in combination with ferritin slightly improved prediction (adjusted R2 = 0.731). A cut-off point of 11% hypochromic erythrocytes reached a high specificity (90%), but was less sensitive (77%).

  8. The dormant blood microbiome in chronic, inflammatory diseases

    PubMed Central

    Potgieter, Marnie; Bester, Janette; Kell, Douglas B.; Pretorius, Etheresia

    2015-01-01

    Blood in healthy organisms is seen as a ‘sterile’ environment: it lacks proliferating microbes. Dormant or not-immediately-culturable forms are not absent, however, as intracellular dormancy is well established. We highlight here that a great many pathogens can survive in blood and inside erythrocytes. ‘Non-culturability’, reflected by discrepancies between plate counts and total counts, is commonplace in environmental microbiology. It is overcome by improved culturing methods, and we asked how common this would be in blood. A number of recent, sequence-based and ultramicroscopic studies have uncovered an authentic blood microbiome in a number of non-communicable diseases. The chief origin of these microbes is the gut microbiome (especially when it shifts composition to a pathogenic state, known as ‘dysbiosis’). Another source is microbes translocated from the oral cavity. ‘Dysbiosis’ is also used to describe translocation of cells into blood or other tissues. To avoid ambiguity, we here use the term ‘atopobiosis’ for microbes that appear in places other than their normal location. Atopobiosis may contribute to the dynamics of a variety of inflammatory diseases. Overall, it seems that many more chronic, non-communicable, inflammatory diseases may have a microbial component than are presently considered, and may be treatable using bactericidal antibiotics or vaccines. PMID:25940667

  9. The dormant blood microbiome in chronic, inflammatory diseases.

    PubMed

    Potgieter, Marnie; Bester, Janette; Kell, Douglas B; Pretorius, Etheresia

    2015-07-01

    Blood in healthy organisms is seen as a 'sterile' environment: it lacks proliferating microbes. Dormant or not-immediately-culturable forms are not absent, however, as intracellular dormancy is well established. We highlight here that a great many pathogens can survive in blood and inside erythrocytes. 'Non-culturability', reflected by discrepancies between plate counts and total counts, is commonplace in environmental microbiology. It is overcome by improved culturing methods, and we asked how common this would be in blood. A number of recent, sequence-based and ultramicroscopic studies have uncovered an authentic blood microbiome in a number of non-communicable diseases. The chief origin of these microbes is the gut microbiome (especially when it shifts composition to a pathogenic state, known as 'dysbiosis'). Another source is microbes translocated from the oral cavity. 'Dysbiosis' is also used to describe translocation of cells into blood or other tissues. To avoid ambiguity, we here use the term 'atopobiosis' for microbes that appear in places other than their normal location. Atopobiosis may contribute to the dynamics of a variety of inflammatory diseases. Overall, it seems that many more chronic, non-communicable, inflammatory diseases may have a microbial component than are presently considered, and may be treatable using bactericidal antibiotics or vaccines.

  10. Predicting response to treatment in chronic inflammatory demyelinating polyradiculoneuropathy.

    PubMed

    Chan, Y-C; Allen, D C; Fialho, D; Mills, K R; Hughes, R A C

    2006-01-01

    To discover whether Inflammatory Neuropathy Cause and Treatment Group (INCAT) electrophysiological criteria for demyelinating neuropathy predict response to immunotherapy in chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). This was a retrospective case note study of patients who had attended Guy's Hospital Peripheral Nerve Clinic between January 2001 and March 2004, been diagnosed as having CIDP, and given treatment with corticosteroids, intravenous immunoglobulin (IVIg), or plasma exchange (PE). Patients' nerve conduction studies (NCS) were reviewed for evidence of demyelination and whether the abnormalities fulfilled modified INCAT electrophysiological criteria. Patients whose NCS fulfilled the criteria were assigned to the neurophysiologically definite CIDP group, while those that did not were labelled as neurophysiologically probable CIDP. Responses to any of the three immunotherapy agents were compared between the two groups. Out of 50 patients, 27 (54%) were classified as neurophysiologically definite and 23 (46%) as neurophysiologically probable CIDP patients. Twenty (74%) neurophysiologically definite and 17 (73.9%) neurophysiologically probable CIDP patients responded to treatment. INCAT electrophysiological criteria did not predict a higher rate of response to immunotherapy. Neurophysiologically probable CIDP patients should be given a trial of immunotherapy.

  11. Predicting response to treatment in chronic inflammatory demyelinating polyradiculoneuropathy

    PubMed Central

    Chan, Y‐C; Allen, D C; Fialho, D; Mills, K R; Hughes, R A C

    2006-01-01

    Objective To discover whether Inflammatory Neuropathy Cause and Treatment Group (INCAT) electrophysiological criteria for demyelinating neuropathy predict response to immunotherapy in chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). Methods This was a retrospective case note study of patients who had attended Guy's Hospital Peripheral Nerve Clinic between January 2001 and March 2004, been diagnosed as having CIDP, and given treatment with corticosteroids, intravenous immunoglobulin (IVIg), or plasma exchange (PE). Patients' nerve conduction studies (NCS) were reviewed for evidence of demyelination and whether the abnormalities fulfilled modified INCAT electrophysiological criteria. Patients whose NCS fulfilled the criteria were assigned to the neurophysiologically definite CIDP group, while those that did not were labelled as neurophysiologically probable CIDP. Responses to any of the three immunotherapy agents were compared between the two groups. Results Out of 50 patients, 27 (54%) were classified as neurophysiologically definite and 23 (46%) as neurophysiologically probable CIDP patients. Twenty (74%) neurophysiologically definite and 17 (73.9%) neurophysiologically probable CIDP patients responded to treatment. Conclusions INCAT electrophysiological criteria did not predict a higher rate of response to immunotherapy. Neurophysiologically probable CIDP patients should be given a trial of immunotherapy. PMID:16361609

  12. Associations of physical activity energy expenditure with nutritional-inflammatory markers in hemodialysis patients.

    PubMed

    Santos, Clarcson P; Silva, Luciana F; Lopes, Marcelo B; Martins, Márcia T S; Kraychete, Angiolina C; Silva, Fernanda A; Martins, Maria T S; Matos, Cácia M; Lopes, Gildete B; Lopes, Antonio A

    2017-08-11

    Sedentariness, high inflammation status and malnutrition are highly prevalent in end-stage kidney disease patients on maintenance hemodialysis (MHD). This study investigated associations of weekly physical activity energy expenditure (PAEE) with clinical and anthropometric markers of nutrition and inflammation. The analysis was performed using baseline cross-sectional data of 640 patients enrolled in the prospective cohort "The Prospective Study of the Prognosis of Patients Treated Chronically by Hemodialysis" (PROHEMO) developed in Salvador, BA, Brazil. The long version of the International Physical Activity Questionnaire was used to determine a summary measure of PAEE, the metabolic equivalent of task (MET), taking into account physical activities related to occupation, recreation, travel, sports, and housework. PAEE was the predictor variable. To assess associations of PAEE with outcomes, the sex-age-specific median MET was used. The malnutrition-inflammation score (MIS) with range of 0 to 30 (higher is worse), conicity index as indicator of abdominal adiposity and C-reactive protein (CRP) were the nutritional-inflammatory outcomes. The mean age of the patients was 48.9 ± 13.8 y, 60.3% were males, 16.7% diabetic, 88.1% nonwhite. In multivariable logistic regression models with adjustments for sociodemographic variables and comorbidities, PAEE ≤median was associated with MIS ≥6 (odds ratio [OR] = 1.57; 95% confidence interval [CI] = 1.08, 2.29), conicity index ≥1.3 (OR = 1.52, 95% CI = 1.03, 2.23) and CRP >1.30 mg/dL (OR = 1.69, 95% CI = 1.08, 2.84). Greater physical activity assessed by PAEE was associated with indicators of better nutritional and inflammation status. These results indicate opportunities for improving outcomes in MHD patients by counseling and treatment intervention.

  13. Coagulation factor VII and inflammatory markers in patients with coronary heart disease.

    PubMed

    Ekström, Mattias; Silveira, Angela; Bennermo, Marie; Eriksson, Per; Tornvall, Per

    2007-07-01

    To further elucidate the connection between inflammation and factor VII (FVII) taking genetic variation in the FVII locus into account, we have examined 387 patients after myocardial infarction and 387 age-matched and sex-matched healthy control individuals. Circulating levels of C-reactive protein, FVII antigen (FVIIag), activated FVII (FVIIa), fibrinogen and interleukin-6 were analysed and all subjects were genotyped for the Arg353Gln polymorphism in the FVII locus. Plasma concentrations of C-reactive protein, fibrinogen, and interleukin-6 were higher among patients than control individuals. FVIIag was lower in the patient group, but for FVIIa there was no difference between the two groups. Among the inflammatory markers, only C-reactive protein indicated a weak nonlinear association with FVII. No significant difference in frequency of the Gln allele was observed between patients and control individuals but the presence of the Gln allele was associated with lower plasma levels of FVIIag and FVIIa in both groups. The low-grade chronic inflammation seen 3 months after myocardial infarction is not of major importance for the variation in plasma concentration of FVII. The presence of the Gln allele in the Arg353Gln polymorphism in the FVII locus did not differ between patients and control individuals but was associated with lower plasma levels of FVIIag and FVIIa that could have a protective effect against myocardial infarction. To further elucidate these facts, a prospective study should be performed to reduce the risk of a possible selection bias due to coronary heart disease death seen in retrospective case-control studies.

  14. Calcific aortic stenosis and its correlation with a novel inflammatory marker, the lymphocyte/monocyte ratio.

    PubMed

    Efe, Tolga Han; Gayretli Yayla, Kadriye; Yayla, Cagri; Ertem, Ahmet Goktug; Cimen, Tolga; Erken Pamukcu, Hilal; Bilgin, Murat; Erat, Mehmet; Dogan, Mehmet; Yeter, Ekrem

    2016-11-01

    Calcific aortic valve disease, a chronic progressive disorder, is the leading cause of valve replacement among elderly patients. The lymphocyte/monocyte ratio has been recently put forward as an inflammatory marker of relevance in several cancers as well as in cardiovascular disease. This study aims to assess the correlation between severity of calcific aortic stenosis and the lymphocyte/monocyte ratio. The study retrospectively included 178 patients with a diagnosis of calcific aortic stenosis and 139 age- and gender-matched controls. The patients were divided into two groups according to the severity of aortic stenosis: mild-to-moderate and severe. An inverse correlation was discerned between the severity of the aortic stenosis process (mean gradient) and the lymphocyte/monocyte ratio (r=-0.232, p=0.002). The lymphocyte/monocyte ratio was observed to decrease as the severity of aortic stenosis increased (p<0.001) in the group with severe aortic stenosis compared with the mild-to-moderate aortic stenosis and control groups (p<0.001, p=0.005 respectively), and in the group with mild-to-moderate aortic stenosis compared with the control group (p=0.003). Multivariate regression analysis revealed that the lymphocyte/monocyte ratio was independently related to the severity of calcific aortic stenosis (p=0.003). The present study demonstrated the existence of a statistically significant inverse relationship between severity of calcific aortic stenosis and the lymphocyte/monocyte ratio. The study also revealed that the lymphocyte/monocyte ratio was significantly related to the severity of the aortic valve stenosis process. Copyright © 2016 Sociedade Portuguesa de Cardiologia. Publicado por Elsevier España, S.L.U. All rights reserved.

  15. Effects of presurgical exercise training on systemic inflammatory markers among patients with malignant lung lesions.

    PubMed

    Jones, Lee W; Eves, Neil D; Peddle, Carolyn J; Courneya, Kerry S; Haykowsky, Mark; Kumar, Vikaash; Winton, Timothy W; Reiman, Tony

    2009-04-01

    Systemic inflammation plays an important role in the initiation, promotion, and progression of lung carcinogenesis. The effects of interventions to lower inflammation have not been explored. Accordingly, we conducted a pilot study to explore the effects of exercise training on changes in biomarkers of systemic inflammation among patients with malignant lung lesions. Using a single-group design, 12 patients with suspected operable lung cancer were provided with structured exercise training until surgical resection. Participants underwent cardiopulmonary exercise testing, 6 min walk testing, pulmonary function testing, and blood collection at baseline and immediately prior to surgical resection. Systemic inflammatory markers included intracellular adhesion molecule (ICAM)-1, macrophage inflammatory protein-1alpha, interleukin (IL)-6, IL-8, monocyte chemotactic protein-1, C-reactive protein, and tumor necrosis factor-alpha. The overall exercise adherence rate was 78%, with patients completing a mean of 30 +/- 25 sessions. Mean peak oxygen consumption increased 2.9 mL.kg-1.min-1 from baseline to presurgery (p = 0.016). Results indicate that exercise training resulted in a significant reduction in ICAM-1 (p = 0.041). Changes in other inflammatory markers did not reach statistical significance. Change in cardiorespiratory fitness was not associated with change in systemic inflammatory markers. This exploratory study provides an initial step for future studies to elucidate the potential role of exercise, as well as identify the underlying mechanisms of action, as a means of modulating the relationship between inflammation and cancer pathogenesis.

  16. Consumption of coffee or caffeine and serum concentration of inflammatory markers: a systematic review.

    PubMed

    Clrs, Paiva; Bts, Beserra; Ceg, Reis; Jg, Dorea; Thm, Costa; Aa, Amato

    2017-10-02

    Coffee consumption is associated with reduced risk of conditions that share low-grade inflammation as their physiopathological basis. We therefore summarized the effects of coffee or coffee components on serum levels of inflammatory markers. Clinical trials assessing the effect of coffee, caffeine or other coffee components on inflammatory markers were searched without restriction to publication date. Fifteen studies (8 involving coffee and 7 caffeine) were included. Increased adiponectin levels were found in four of seven trials comparing filtered coffee/caffeinated coffee with placebo or comparing its levels at baseline and after consumption of medium or dark roasted coffee, but no change was seen in caffeine trials. None of the five studies assessing the effects of coffee found changes in C-reactive protein (CPR), but one out of three trials found decreased CPR levels in response to caffeine. Interleukin (IL)-6 was increased by caffeinated coffee compared with placebo in one of four coffee trials, and by caffeine in three out of five studies. Caffeine increased IL-10 levels in two of three trials. These data suggest a predominant anti-inflammatory action of coffee but not of caffeine consumption. Moreover, the proinflammatory and anti-inflammatory responses to caffeine point to its complex effects on the inflammatory response.

  17. Inflammatory markers and risk of hip fracture in older white women: the study of osteoporotic fractures.

    PubMed

    Barbour, Kamil E; Lui, Li-Yung; Ensrud, Kristine E; Hillier, Teresa A; LeBlanc, Erin S; Ing, Steven W; Hochberg, Marc C; Cauley, Jane A

    2014-09-01

    Hip fractures are the most devastating consequence of osteoporosis and impact 1 in 6 white women leading to a two- to threefold increased mortality risk in the first year. Despite evidence of inflammatory markers in the pathogenesis of osteoporosis, few studies have examined their effect on hip fracture. To determine if high levels of inflammation increase hip fracture risk and to explore mediation pathways, a case-cohort design nested in a cohort of 4709 white women from the Study of Osteoporotic Fractures was used. A random sample of 1171 women was selected as the subcohort (mean age 80.1 ± 4.2 years) plus the first 300 women with incident hip fracture. Inflammatory markers interleukin-6 (IL-6) and soluble receptors (SR) for IL-6 (IL-6 SR) and tumor necrosis factor (TNF SR1 and TNF SR2) were measured, and participants were followed for a median (interquartile range) of 6.3 (3.7, 6.9) years. In multivariable models, the hazard ratio (HR) of hip fracture for women in the highest inflammatory marker level (quartile 4) was 1.64 (95% confidence interval [CI], 1.09-2.48, p trend = 0.03) for IL-6 and 2.05 (95% CI, 1.35-3.12, p trend <0.01) for TNF SR1 when compared with women in the lowest level (quartile 1). Among women with 2 and 3-4 inflammatory markers in the highest quartile, the HR of hip fracture was 1.51 (95% CI, 1.07-2.14) and 1.42 (95% CI, 0.87-2.31) compared with women with zero to one marker(s) in the highest quartile (p trend = 0.03). After individually adjusting for seven potential mediators, cystatin-C (a biomarker of renal function) and bone mineral density (BMD) attenuated HRs among women with the highest inflammatory burden by 64% and 50%, respectively, suggesting a potential mediating role. Older white women with high inflammatory burden are at increased risk of hip fracture in part due to poor renal function and low BMD. © 2014 American Society for Bone and Mineral Research.

  18. Impact of chronic lead exposure on selected biological markers.

    PubMed

    Jangid, Ambica P; John, P J; Yadav, D; Mishra, Sandhya; Sharma, Praveen

    2012-01-01

    Lead poisoning remains a major problem in India due to the lack of awareness of its ill effects among the clinical community. Blood lead, δ-aminolevulinic acid dehydratase (δ-ALAD) and zinc protoporphyrin (ZPP) concentrations are widely used as biomarkers for lead toxicity The present study was designed to determine the impact of chronic lead exposure on selected biological markers. A total of 250 subjects, of both sexes, ranging in age from 20 to 70 years, were recruited. On the basis of BLLs, the subjects were categorized into four groups: Group A (BLL: 0-10 μg/dl), Group B (BLL: 10-20 μg/dl). Group C (BLL: 20-30 μg/dl) and Group D (BLL: 30-40 μg/dl) having BLLs of 3.60 ± 2.71 μg/dl, 15.21 ± 2.65 μg/dl, 26.82 ± 2.53 μg/dl and 36.38 ± 2.83 μg/dl, respectively. Significant changes in biological markers due to elevated BLLs were noted. The relation of BLL and biological markers to demographic characteristics such as sex, habits, diet and substances abuse (smoking effect) were also studied in the present investigation. Males, urban population, non-vegetarians, and smokers had higher blood lead levels. δ-ALAD activity was found to be significantly lower with increased BLL (P < 0.001), while the ZPP level was significantly higher with increased BLL (P < 0.001). Further, BLL showed a negative correlation with δ-ALAD (r = -0.425, P < 0.001, N = 250) and a positive correlations with ZPP (r = 0.669, P < 0.001, N = 250). Chronic lead exposure affects the prooxidant-antioxidant equilibrium leading to cellular oxidative stress.

  19. Idiopathic chronic inflammatory demyelinating polyneuropathy: an epidemiological study in Italy

    PubMed Central

    Chiò, A; Cocito, D; Bottacchi, E; Buffa, C; Leone, M; Plano, F; Mutani, R; Calvo, A

    2007-01-01

    Aim The clinical and epidemiological characteristics of chronic inflammatory demyelinating polyneuropathy (CIDP) in an Italian population were assessed. Subjects and methods All subjects with a diagnosis of demyelinating neuropathy after 1990 in Piemonte and Valle d'Aosta (4 334 225 inhabitants) were considered. The diagnosis of CIDP was based on the research criteria of the American Academy of Neurology. 165 of 294 patients met the diagnostic criteria. Results The crude prevalence rate was 3.58/100 000 population (95% CI 3.02 to 4.20). At the prevalence day, 76 (49.0%) cases had definite, 67 (43.2%) probable and 12 (7.7%) possible CIDP; disability was mild in 105 (67.7%) cases, moderate in 32 (20.6%) and severe in 18 (11.6%). The course was remitting–relapsing in 40 cases (25.8%), chronic progressive in 96 (61.9%) and monophasic in 19 (12.3%). Considering the 95 patients whose disorder presented in the period 1995–2001, the mean annual crude incidence rate was 0.36/100 000 population (95% CI 0.29 to 0.44), with a male to female ratio of 2.3:1. 14 cases were affected by diabetes mellitus. In multivariate analysis, factors related to severe disability at the prevalence day were: age>60 years; failure of immunomodulating therapies at the time of diagnosis; worse disability at nadir; and chronic course. Conclusion Incidence and prevalence rates of CIDP in Italy were higher than those observed in most previous studies. At the prevalence day, more than 80% of cases had a mild or moderate disability, indicating either a good response to immunomodulating therapy or a tendency of CIDP to have a mild course in most cases. PMID:17494979

  20. DISREGULATION OF INFLAMMATORY RESPONSES BY CHRONIC CIRCADIAN DISRUPTION

    PubMed Central

    Castanon-Cervantes, Oscar; Wu, Mingwei; Ehlen, J. Christopher; Paul, Ketema; Gamble, Karen L.; Johnson, Russell L.; Besing, Rachel C.; Menaker, Michael; Gewirtz, Andrew T.; Davidson, Alec J.

    2010-01-01

    Circadian rhythms modulate nearly every mammalian physiological process. Chronic disruption of circadian timing in shift work or during chronic jet lag in animal models leads to a higher risk of several pathologies. Many of these conditions in both shift workers and experimental models share the common risk factor of inflammation. Here we show that experimentally-induced circadian disruption altered innate immune responses. Endotoxemic shock induced by LPS was magnified leading to hypothermia and death after 4 consecutive weekly 6h phase-advances of the light-dark schedule, with 89% mortality compared with 21% in unshifted control mice. This may be due to a heightened release of pro-inflammatory cytokines in response to LPS treatment in shifted animals. Isolated peritoneal macrophages harvested from shifted mice exhibited a similarly heightened response to LPS in vitro, indicating that these cells are a target for jet lag. Sleep deprivation and stress are known to alter immune function and are potential mediators of the effects we describe. However polysomnographic recording in mice exposed to the shifting schedule revealed no sleep loss, and stress measures were not altered in shifted mice. In contrast, we observed altered or abolished rhythms in the expression of clock genes in the central clock, liver, thymus and peritoneal macrophages in mice after chronic jet lag. We conclude that circadian disruption, but not sleep loss or stress, are associated with jet lag-related disregulation of the innate immune system. Such immune changes might be a common mechanism for the myriad negative health effects of shift work. PMID:20944004

  1. Relationship of inflammatory markers and pain in patients with head and neck cancer prior to anticancer therapy

    PubMed Central

    Oliveira, K.G.; von Zeidler, S.V.; Lamas, A.Z.; de Podestá, J.R.V.; Sena, A.; Souza, E.D.; Lenzi, J.; Lemos, E.M.; Gouvea, S.A.; Bissoli, N.S.

    2014-01-01

    Pain is a common symptom in patients with cancer, including those with head and neck cancer (HNC). While studies suggest an association between chronic inflammation and pain, levels of inflammatory cytokines, such as C-reactive protein (CRP) and tumor necrosis factor-alpha (TNF-α), have not been correlated with pain in HNC patients who are not currently undergoing anticancer treatment. The purpose of this study was to examine the relationship between these inflammatory markers and perceived pain in HNC patients prior to anticancer therapy. The study group consisted of 127 HNC patients and 9 healthy controls. Pain was assessed using the Brief Pain Inventory (BPI), and serum levels of CRP and TNF-α were determined using the particle-enhanced turbidimetric immunoassay (PETIA) and ELISA techniques, respectively. Patients experiencing pain had significantly higher levels of CRP (P<0.01) and TNF-α (P<0.05) compared with controls and with patients reporting no pain. There were significantly positive associations between pain, CRP level, and tumor stage. This is the first study to report a positive association between perceived pain and CRP in HNC patients at the time of diagnosis. The current findings suggest important associations between pain and inflammatory processes in HNC patients, with potential implications for future treatment strategies. PMID:25003634

  2. Pro-inflammatory cytokines: Useful markers for the diagnosis of canine mammary tumours?

    PubMed

    Andaluz, Ana; Yeste, Marc; Rodríguez-Gil, Joan E; Rigau, Teresa; García, Félix; Rivera del Álamo, Maria Montserrat

    2016-04-01

    The aim of the present study was to analyse the expression of 60 pro-inflammatory cytokines as possible markers of malignancy in canine mammary tumours using a human cytokine antibody array. The cytokines were grouped into two different categories: (1) cytokines in which expression indicated the presence of a mammary tumour and (2) cytokines in which expression differentiated between simple mammary adenoma, tubulopapillary carcinoma or complex carcinoma. These data suggest that specific pro-inflammatory cytokines could be useful as tools for the diagnosis of canine mammary tumours. Copyright © 2016 Elsevier Ltd. All rights reserved.

  3. Longitudinal Impact of Smoking and Smoking Cessation on Inflammatory Markers of Cardiovascular Disease Risk.

    PubMed

    King, Cecile C; Piper, Megan E; Gepner, Adam D; Fiore, Michael C; Baker, Timothy B; Stein, James H

    2017-02-01

    To evaluate longitudinal changes in 6 inflammatory markers that predict cardiovascular disease events among smokers making a quit attempt and to characterize their cross-sectional associations between smoking and smoking heaviness. In a longitudinal cohort study of contemporary smokers (n=1652), we evaluated (1) independent associations of smoking heaviness markers (exhaled carbon monoxide, cigarettes/d, pack-years) with inflammatory markers (C-reactive protein, D-dimer, fibrinogen, urinary F2 isoprostane:creatinine [F2:Cr] ratio, white blood cell [WBC] count, myeloperoxidase) and (2) the effects of smoking cessation and continued smoking on these inflammatory markers after 1 year, among the 888 smokers who made an aided quit attempt as part of a randomized comparative effectiveness trial or standard care. There were strong, independent associations between smoking heaviness markers and the F2:Cr ratio, WBC, and myeloperoxidase (all Padj<0.001), but not high-sensitivity C-reactive protein, D-dimer, or fibrinogen. Participants were mean (SD) 49.6 years old (11.6), 54% women, 34% non-white, and smoked 16.8 cigarettes/d (8.5) for 27.3 pack-years (18.6). After 1 year, the 344 successful abstainers gained more weight (4.0 [6.0] versus 0.4 [5.7] pounds; P<0.001) and had larger increases in insulin resistance scores (P=0.02) than continuing smokers. Despite these increases, abstainers had significant decreases in F2:Cr ratio (P<0.001) and WBC counts (P<0.001). Changes in other markers were not related to quitting. Smoking heaviness is associated with increased F2:Cr ratio, myeloperoxidase, and WBC counts. Cessation improves the F2:Cr ratio and WBC counts independent of weight change, suggesting reduced inflammation related to less oxidant stress. © 2016 American Heart Association, Inc.

  4. A case of chronic inflammatory demyelinating polyneuropathy presented with unilateral ptosis.

    PubMed

    Izadi, Sadegh; Karamimagham, Sina; Poursadeghfard, Maryam

    2014-01-01

    Chronic Inflammatory Demyelinating Polyneuropathy is an autoimmune disease with progressive and relapsing courses. The main clinical presentations are diffuse deep tendon hyporeflexia or areflexia and symmetric proximal-distal muscles weakness. Myasthenia gravis is also an immune mediated disease with fluctuating ocular and bulbar symptoms and sometimes weakness. Although both myasthenia gravis and chronic inflammatory demyelinating polyneuropathy are immune mediated disorders, clinical presentations are obviously different in the two diseases. Herein, we will report a case of chronic inflammatory demyelinating polyneuropathy who presented with isolated unilateral ptosis. Initially, the patient was managed as ocular type of myasthenia gravis, but after progression to general limb weakness and areflexia, the diagnosis of chronic inflammatory demyelinating polyneuropathy was made. Although unilateral ptosis is a typical feature of myasthenia gravis, it may be seen as the first presentation of chronic inflammatory demyelinating polyneuropathy as well which mimics myasthenia gravis disease.

  5. Inflammatory and Metabolic Alterations of Kager's Fat Pad in Chronic Achilles Tendinopathy

    PubMed Central

    Fredberg, Ulrich; Kjær, Søren G.; Quistorff, Bjørn; Langberg, Henning; Hansen, Jacob B.

    2015-01-01

    Background Achilles tendinopathy is a painful inflammatory condition characterized by swelling, stiffness and reduced function of the Achilles tendon. Kager’s fat pad is an adipose tissue located in the area anterior to the Achilles tendon. Observations reveal a close physical interplay between Kager’s fat pad and its surrounding structures during movement of the ankle, suggesting that Kager’s fat pad may stabilize and protect the mechanical function of the ankle joint. Aim The aim of this study was to characterize whether Achilles tendinopathy was accompanied by changes in expression of inflammatory markers and metabolic enzymes in Kager’s fat pad. Methods A biopsy was taken from Kager’s fat pad from 31 patients with chronic Achilles tendinopathy and from 13 healthy individuals. Gene expression was measured by reverse transcription-quantitative PCR. Focus was on genes related to inflammation and lipid metabolism. Results Expression of the majority of analyzed inflammatory marker genes was increased in patients with Achilles tendinopathy compared to that in healthy controls. Expression patterns of the patient group were consistent with reduced lipolysis and increased fatty acid β-oxidation. In the fat pad, the pain-signaling neuropeptide substance P was found to be present in one third of the subjects in the Achilles tendinopathy group but in none of the healthy controls. Conclusion Gene expression changes in Achilles tendinopathy patient samples were consistent with Kager’s fat pad being more inflamed than in the healthy control group. Additionally, the results indicate an altered lipid metabolism in Kager’s fat pad of Achilles tendinopathy patients. PMID:25996876

  6. [THE CHARACTERISTICS OF MORPHOLOGY OF BIOFILM OF PERIODONTIUM UNDER INFLAMMATORY DISEASES OF GUMS (CHRONIC CATARRHAL GINGIVITIS, CHRONIC PERIODONTITIS, CANDIDA-ASSOCIATED PERIODONTITIS) ACCORDING RESULTS OF ELECTRONIC MICROSCOPY].

    PubMed

    Ippolitov, E V; Didenko, L V; Tzarev, V N

    2015-12-01

    The study was carried out to analyze morphology of biofilm of periodontium and to develop electronic microscopic criteria of differentiated diagnostic of inflammatory diseases of gums. The scanning electronic microscopy was applied to analyze samples of bioflm of periodont from 70 patients. Including ten patients with every nosologic form of groups with chronic catarrhal periodontitis. of light, mean and severe degree, chronic catarrhal gingivitis, Candida-associated paroperiodontitis and 20 healthy persons with intact periodontium. The analysis was implemented using dual-beam scanning electronic microscope Quanta 200 3D (FEI company, USA) and walk-through electronic micJEM 100B (JEOL, Japan). To detect marker DNA of periodont pathogenic bacteria in analyzed samples the kit of reagentsfor polymerase chain reaction "MultiDent-5" ("GenLab", Russia). The scanning electronic microscopy in combination with transmission electronic microscopy and polymerase chain reaction permits analyzing structure, composition and degree of development of biofilm of periodontium and to apply differentiated diagnostic of different nosologic forms of inflammatory diseases of periodontium, including light form of chronic periodontitis and gingivitis. The electronic microscopical indications of diseases ofperiodontium of inflammatory character are established: catarrhal gingivitis, (coccal morphological alternate), chronic periodontitis (bacillary morphological alternate), Candida-associated periodontitis (Candida morphological alternate of biofilm ofperiodontium).

  7. [ASSOCIATION OF POLYMORPHIC MARKERS IN GENES OF INNATE IMMUNITY IN PATIENTS WITH PERIODONTITIS AND INFLAMMATORY DISEASES OF UPPER RESPIRATORY TRACT].

    PubMed

    Sarkisyan, N G; Gankovskaya, L V; Tuzankina, I A; Svitich, O A; Ron, G I; Shershnev, V N; Kolyadina, O N; Dolgikh, M A

    2016-01-01

    Search of association of polymorphisms in DEFB1, IL-10, TNF-α and TLR2 genes with development of chronic generalized periodontitis in representatives of Ural region (Caucasian race). 142 patients, that were split into 3 groups, took part in the study: a group of patients with periodontitis, a group with frequent inflammatory disease of upper respiratory tract and a comparison group--healthy donors. A study of polymorphic markers was carried out: DEFB1 (-44G/C), DEFB1 (-20A/G), IL-10 (-1082.A/G), TNF-α (-308 G/A), Arg753Gln and Arg677Trp using PCR in real time mode. Association of infectious pathology ofupper respiratory tract and development of periodontitis diseases with markers in DEFB1 (-44G/C) and Arg753Gln and Arg677Trp genes was determined. Significant differences in distribution of genotypes and alleles of genes IL-10 and TNF-α in the group of patients with periodontitis and comparison group were not detected. DEFB1 (-44G/C) polymorphism can be examined as a marker of periodontitis development risk.

  8. Effects of prandial challenge on triglyceridemia, glycemia, and pro-inflammatory activity in persons with chronic paraplegia.

    PubMed

    Ellenbroek, Dennis; Kressler, Jochen; Cowan, Rachel E; Burns, Patricia A; Mendez, Armando J; Nash, Mark S

    2015-07-01

    Exaggerated postprandial lipemia has been reported after spinal cord injury (SCI). We examined metabolite and accompanying pro-inflammatory biomarker responses to repeat feeding of typical high-fat meals in individuals with chronic paraplegia. Descriptive trial. Metabolites (triglycerides, glucose, and insulin) and inflammatory biomarkers (interleukin-6 and high-sensitivity C-reactive protein (hsCRP)) were measured under fasting conditions in 11 recreationally active individuals with chronic (>1 year) paraplegia. Subjects received high-fat meals at time point 0 and again at minute 240. Antecubital venous blood was obtained at time points -30 (fasting), 0 (first meal), 30, 60, 90, 120, 240 (second meal), 360, and 480 minutes. Correlations were examined among the study variables. Exploratory subgroup analysis was performed for subjects with levels of postprandial glucose greater than >200 mg/dl. Triglycerides showed a significant rise 4 hours after eating. Basal inflammatory markers were elevated, and did not undergo additional change during the testing. Additionally, subjects with excessive postprandial glucose responses showed higher hsCRP levels than those having typical glucose responses both for fasting (11.8 ± 6.5 vs. 2.9 ± 2.7 mg/l, P = 0.064) and postprandial (11.1 ± 4.9 vs. 3.7 ± 3.8 mg/l, P = 0.018) values. Despite elevations in metabolic response markers, inflammatory markers did not change significantly after consumption of population-representative (i.e. hypercaloric) mixed-nutrient meals. Levels of fasting CRP in the high-risk range are consistent with other reports in persons with SCI and continue to pose concern for their cardiovascular disease risk. The possible association between postprandial metabolic responses and inflammatory states warrants further investigation to identify individual component risks for this secondary health hazard.

  9. Plasma n-3 and n-6 fatty acids and inflammatory markers in Chinese vegetarians.

    PubMed

    Yu, Xiaomei; Huang, Tao; Weng, Xiumei; Shou, Tianxing; Wang, Qiang; Zhou, Xiaoqiong; Hu, Qinxin; Li, Duo

    2014-09-29

    Polyunsaturated fatty acid (PUFA) intake favorably affects chronic inflammatory-related diseases such as cardiovascular disease; however, the relationship between the PUFA and inflammatory factors in the healthy vegetarians were not clear. We aimed to investigate the plasma fatty acids status, and its association with plasma inflammatory factors in Chinese vegetarians and omnivores. A total of 89 male vegetarians and 106 male omnivores were participated the study. Plasma concentrations of inflammatory factors were detected by ELISA, and as standard methods fatty acids were extracted and determined by chromatography. Compared with omnivores, vegetarians have significant higher interleukin-6 (IL-6), plasma n-6 PUFA, n-6/n-3, and 18:3n-3; while they have significant lower leukotriene B4 (LTB4), cyclo-oxygenase-2 (COX2) and prostaglandin E2 (PGE2), 20:5n-3, 22:5n-3, 22:6n-3, and n-3 PUFA. In vegetarians, plasma 20:4n-6 was significant positively related to TNF-α. LTB4 was significantly positively related to plasma 22:6n-3, and negatively associated with n-6 PUFA. Vegetarians have higher plasma n-6 PUFA and IL-6, but lower LTB4, n-3 PUFA, 22:6n-3, COX2 and PGE2 levels. It would seem appropriate for vegetarians to increase their dietary n-3 PUFA, while reduce dietary n-6 PUFA and thus reduce the risk of chronic inflammatory-related diseases.

  10. Anti-oxidative assays as markers for anti-inflammatory activity of flavonoids.

    PubMed

    Chanput, Wasaporn; Krueyos, Narumol; Ritthiruangdej, Pitiporn

    2016-11-01

    The complexity of in vitro anti-inflammatory assays, the cost and time consumed, and the necessary skills can be a hurdle to apply to promising compounds in a high throughput setting. In this study, several antioxidative assays i.e. DPPH, ABTS, ORAC and xanthine oxidase (XO) were used to examine the antioxidative activity of three sub groups of flavonoids: (i) flavonol: quercetin, myricetin, (ii) flavanone: eriodictyol, naringenin (iii) flavone: luteolin, apigenin. A range of flavonoid concentrations was tested for their antioxidative activities and were found to be dose-dependent. However, the flavonoid concentrations over 50ppm were found to be toxic to the THP-1 monocytes. Therefore, 10, 20 and 50ppm of flavonoid concentrations were tested for their anti-inflammatory activity in lipopolysaccharide (LPS)-stimulated THP-1 monocytes. Expression of inflammatory genes, IL-1β, IL-6, IL-8, IL-10 and TNF-α was found to be sequentially decreased when flavonoid concentration increased. Principle component analysis (PCA) was used to investigate the relationship between the data sets of antioxidative assays and the expression of inflammatory genes. The results showed that DPPH, ABTS and ORAC assays have an opposite correlation with the reduction of inflammatory genes. Pearson correlation exhibited a relationship between the ABTS assay and the expression of three out of five analyzed genes; IL-1β, IL-6 and IL-8. Our findings indicate that ABTS assay can potentially be an assay marker for anti-inflammatory activity of flavonoids.

  11. Soy Food Intake and Circulating Levels of Inflammatory Markers in Chinese Women

    PubMed Central

    Wu, Sheng Hui; Shu, Xiao Ou; Chow, Wong-Ho; Xiang, Yong-Bing; Zhang, Xianglan; Li, Hong-Lan; Cai, Qiuyin; Ji, Bu-Tian; Cai, Hui; Rothman, Nathaniel; Gao, Yu-Tang; Zheng, Wei; Yang, Gong

    2013-01-01

    Background Soy and some of its constituents, such as isoflavones, have been shown to affect the inflammatory process in animal studies. The association between soy food intake and inflammatory markers has not been evaluated adequately in humans. Objective Our aim was to evaluate whether higher intake of soy foods was inversely associated with inflammatory markers in 1,005 middle-aged Chinese women. Design In this cross-sectional study, dietary intake of soy foods was assessed by a validated food frequency questionnaire and by a 24-hour recall when biospecimens were procured. A general linear model was used to estimate the geometric means of selected inflammatory markers, including interleukin-6 (IL-6), IL-1β, tumor necrosis factor-α (TNFα), soluble IL-6 receptor, soluble GP130, soluble TNF receptors 1 and 2, and C-reactive protein, across categories of soy food intake after adjusting for age, lifestyle and dietary factors, and history of infectious or inflammation-related diseases. Results We found that multivariable-adjusted geometric mean concentrations of IL-6 and TNFα were inversely associated with quintiles of soy food intake, with a difference between the highest and lowest quintiles of 25.5% for IL-6 (P for trend = 0.008) and 14% for TNFα (P for trend = 0.04). Similar inverse associations were found for TNFα (P for trend = 0.003), soluble TNF receptor 1 (P for trend=0.01), soluble TNF receptor 2 (P for trend=0.02), IL-1β (P for trend=0.05), and IL-6 (P for trend=0.04) when soy food consumption was assessed by the frequency of consumption in the preceding 24 hours. No significant associations were found for other markers studied. Conclusions This study suggests that soy food consumption is related to lower circulating levels of IL-6, TNFα, and soluble TNF receptors 1 and 2 in Chinese women. PMID:22889631

  12. Prediction of Asthma Exacerbations in Children by Innovative Exhaled Inflammatory Markers: Results of a Longitudinal Study

    PubMed Central

    van Vliet, Dillys; Alonso, Ariel; Rijkers, Ger; Heynens, Jan; Rosias, Philippe; Muris, Jean; Jöbsis, Quirijn; Dompeling, Edward

    2015-01-01

    Background In asthma management guidelines the primary goal of treatment is asthma control. To date, asthma control, guided by symptoms and lung function, is not optimal in many children and adults. Direct monitoring of airway inflammation in exhaled breath may improve asthma control and reduce the number of exacerbations. Aim 1) To study the use of fractional exhaled nitric oxide (FeNO) and inflammatory markers in exhaled breath condensate (EBC), in the prediction of asthma exacerbations in a pediatric population. 2) To study the predictive power of these exhaled inflammatory markers combined with clinical parameters. Methods 96 asthmatic children were included in this one-year prospective observational study, with clinical visits every 2 months. Between visits, daily symptom scores and lung function were recorded using a home monitor. During clinical visits, asthma control and FeNO were assessed. Furthermore, lung function measurements were performed and EBC was collected. Statistical analysis was performed using a test dataset and validation dataset for 1) conditionally specified models, receiver operating characteristic-curves (ROC-curves); 2) k-nearest neighbors algorithm. Results Three conditionally specified predictive models were constructed. Model 1 included inflammatory markers in EBC alone, model 2 included FeNO plus clinical characteristics and the ACQ score, and model 3 included all the predictors used in model 1 and 2. The area under the ROC-curves was estimated as 47%, 54% and 59% for models 1, 2 and 3 respectively. The k-nearest neighbors predictive algorithm, using the information of all the variables in model 3, produced correct predictions for 52% of the exacerbations in the validation dataset. Conclusion The predictive power of FeNO and inflammatory markers in EBC for prediction of an asthma exacerbation was low, even when combined with clinical characteristics and symptoms. Qualitative improvement of the chemical analysis of EBC may lead to a

  13. Compound 49b Reduces Inflammatory Markers and Apoptosis after Ocular Blast Injury

    DTIC Science & Technology

    2013-09-01

    coherence topography , gross pathology, and optokinetics [9]. In this study of various blast pressures, the authors found only 1 eye after exposure to 26psi...For most ocular trauma studies, work has focused on corneal burns or trauma. However, since it is likely that other ocular targets are affected...warranted. Our findings of increased inflammatory and apoptotic markers after exposure to ocular blast agree with work from corneal burns or

  14. Treatment of chronic inflammatory demyelinating polyneuropathy with pulsed oral steroids.

    PubMed

    Muley, Suraj Ashok; Kelkar, Praful; Parry, Gareth J

    2008-11-01

    Chronic inflammatory demyelinating polyneuropathy (CIDP) is an immune-mediated neuropathy that responds to various immunosuppressive treatments. Oral daily prednisone therapy is effective and inexpensive, but the long-term treatment that is usually necessary leads to serious adverse effects. Consequently, intravenous immunoglobulin and plasma exchange have been widely used to treat CIDP, making treatment expensive and inconvenient. A steroid regimen that reduces adverse effects but preserves efficacy would simplify treatment. Pulsed steroids have nongenomic actions not seen with low-dose steroids, including rapid inhibition of arachidonic acid release and of calcium and sodium cycling across plasma membranes of immune cells. To study the efficacy, safety, and tolerability of pulsed oral methylprednisolone therapy in patients with CIDP. Open-label prospective study. University of Minnesota Neuropathy Center, Minneapolis. Ten patients (3 women and 7 men) with CIDP followed up for at least 22 months. Neuromuscular score and Inflammatory Neuropathy Cause and Treatment (INCAT) disability score were used as outcome measures for efficacy; weight, blood pressure, changes in bone density, and steroid-related adverse effect questionnaire were used as outcome measures for safety. This steroid regimen leads to significant improvement in weakness and disability in all patients treated and to off-treatment remission in 60% of patients. Treatment was fairly well tolerated, and only 1 patient discontinued treatment because of adverse effects. Steroid-induced osteoporosis remained a problem, especially in older patients. Pulsed oral methylprednisolone may be efficacious in the long-term treatment of CIDP and is relatively well tolerated. Remission can be induced in most patients, especially those with a shorter duration of disease.

  15. Atherosclerotic cardiovascular disease in patients with chronic inflammatory joint disorders.

    PubMed

    Agca, R; Heslinga, S C; van Halm, V P; Nurmohamed, M T

    2016-05-15

    Inflammatory joint disorders (IJD), including rheumatoid arthritis (RA), ankylosing spondylitis (ASp) and psoriatic arthritis (PsA), are prevalent conditions worldwide with a considerable burden on healthcare systems. IJD are associated with increased cardiovascular (CV) disease-related morbidity and mortality. In this review, we present an overview of the literature. Standardised mortality ratios are increased in IJD compared with the general population, that is, RA 1.3-2.3, ASp 1.6-1.9 and PsA 0.8-1.6. This premature mortality is mainly caused by atherosclerotic events. In RA, this CV risk is comparable to that in type 2 diabetes. Traditional CV risk factors are more often present and partially a consequence of changes in physical function related to the underlying IJD. Also, chronic systemic inflammation itself is an independent CV risk factor. Optimal control of disease activity with conventional synthetic, targeted synthetic and biological disease-modifying antirheumatic drugs decreases this excess risk. High-grade inflammation as well as anti-inflammatory treatment alter traditional CV risk factors, such as lipids. In view of the above-mentioned CV burden in patients with IJD, CV risk management is necessary. Presently, this CV risk management is still lacking in usual care. Patients, general practitioners, cardiologists, internists and rheumatologists need to be aware of the substantially increased CV risk in IJD and should make a combined effort to timely initiate CV risk management in accordance with prevailing guidelines together with optimal control of rheumatic disease activity. CV screening and treatment strategies need to be implemented in usual care.

  16. Influence of Sleep Deprivation and Circadian Misalignment on Cortisol, Inflammatory Markers, and Cytokine Balance

    PubMed Central

    Wright, Kenneth P.; Drake, Amanda L.; Frey, Danielle J.; Fleshner, Monika; Desouza, Christopher A.; Gronfier, Claude; Czeisler, Charles A.

    2017-01-01

    Cortisol and inflammatory proteins are released into the blood in response to stressors and chronic elevations of blood cortisol and inflammatory proteins may contribute to ongoing disease processes and could be useful biomarkers of disease. How chronic circadian misalignment influences cortisol and inflammatory proteins, however, is largely unknown and this was the focus of the current study. Specifically, we examined the influence of weeks of chronic circadian misalignment on cortisol, stress ratings, and pro- and anti- inflammatory proteins in humans. We also compared the effects of acute total sleep deprivation and chronic circadian misalignment on cortisol levels. Healthy, drug free females and males (N=17) aged 20-41 participated. After three weeks of maintaining consistent sleep-wake schedules at home, six laboratory baseline days and nights, a 40-h constant routine (CR, total sleep deprivation) to examine circadian rhythms for melatonin and cortisol, participants were scheduled to a 25-day laboratory entrainment protocol that resulted in sleep and circadian disruption for eight of the participants. A second constant routine was conducted to reassess melatonin and cortisol rhythms on days 34-35. Plasma cortisol levels were also measured during sampling windows every week and trapezoidal area under the curve (AUC) was used to estimate 24-h cortisol levels. Inflammatory proteins were assessed at baseline and near the end of the entrainment protocol. Acute total sleep deprivation significantly increased cortisol levels (p<0.0001), whereas chronic circadian misalignment significantly reduced cortisol levels (p<0.05). Participants who exhibited normal circadian phase relationships with the wakefulness-sleep schedule showed little change in cortisol levels. Stress ratings increased during acute sleep deprivation (p<0.0001), whereas stress ratings remained low across weeks of study for both the misaligned and synchronized control group. Circadian misalignment

  17. [Evaluation of the concordance between biological markers and clinical activity in inflammatory bowel disease].

    PubMed

    Miranda García, Pablo; Chaparro, María; Gisbert, Javier P

    2015-01-06

    Endoscopy is the gold standard to assess disease severity in inflammatory bowel disease, although it is an invasive procedure. Clinical activity and biological markers have been routinely used to determine disease activity in a non-invasive manner. The aim of this study was to determine concordance between common biological markers (C reactive protein, orosomucoid, erythrocyte sedimentation rate, fibrinogen, platelets, leukocytes, neutrophils and haemoglobin) and clinical activity in inflammatory bowel disease. Consecutive patients with inflammatory bowel disease were included. Clinical activity was evaluated according to the Harvey-Bradshaw index in Crohn's disease and to the partial Mayo score in ulcerative colitis. Serum concentrations of the different biomarkers were analysed. Concordance between clinical activity and elevation of the serological biomarkers was determined using the kappa statistic. In total, 350 patients were included (median age 46 years, Crohn's disease 59%). Eleven percent of patients had clinical activity. Crohn's disease patients had mild clinical activity in 44% of cases, moderate disease in 44% and only 12% of patients had severe clinical activity. In ulcerative colitis, patients had mild, moderate and severe clinical activity in 50, 42 and 8% of cases, respectively. None of the biomarkers included had an acceptable concordance with clinical activity (kappa statistic ≤ 0.30). Concordance between serological biomarkers and clinical activity in inflammatory bowel disease is remarkably low. Copyright © 2013 Elsevier España, S.L.U. All rights reserved.

  18. Chronic Inflammatory Disease and Osteopathy: A Systematic Review

    PubMed Central

    Cicchitti, Luca; Martelli, Marta; Cerritelli, Francesco

    2015-01-01

    Background Chronic inflammatory diseases (CID) are globally highly prevalent and characterized by severe pathological medical conditions. Several trials were conducted aiming at measuring the effects of manipulative therapies on patients affected by CID. The purpose of this review was to explore the extent to which osteopathic manipulative treatment (OMT) can be benefi-cial in medical conditions also classified as CID. Methods This review included any type of experimental study which enrolled sub-jects with CID comparing OMT with any type of control procedure. The search was conducted on eight databases in January 2014 using a pragmatic literature search approach. Two independent re-viewers conducted study selection and data extraction for each study. The risk of bias was evaluated according to the Cochrane methods. Heterogeneity was assessed and meta-analysis performed where possible. Results 10 studies met the inclusion criteria for this review enrolling 386 subjects. The search identified six RCTs, one laboratory study, one cross-over pilot studies, one observation-al study and one case control pilot study. Results suggest a potential effect of osteopathic medicine on patients with medical pathologies associated with CID (in particular Chronic Obstructive Pul-monary Disease (COPD), Irritable Bowel Syndrome, Asthma and Peripheral Arterial Disease) com-pared to no treatment or sham therapy although data remain elusive. Moreover one study showed possible effects on arthritis rat model. Meta-analysis was performed for COPD studies only show-ing no effect of any type of OMT applied versus control. No major side effects were reported by those receiving OMT. Conclusion The present systematic review showed inconsistent data on the effect of OMT in the treatment of medical conditions potentially associated with CID, however the OMT appears to be a safe approach. Further more robust trials are needed to determine the direction and magnitude of the effect of OMT and to

  19. Inflammatory mechanisms in patients with chronic obstructive pulmonary disease.

    PubMed

    Barnes, Peter J

    2016-07-01

    Chronic obstructive pulmonary disease (COPD) is associated with chronic inflammation affecting predominantly the lung parenchyma and peripheral airways that results in largely irreversible and progressive airflow limitation. This inflammation is characterized by increased numbers of alveolar macrophages, neutrophils, T lymphocytes (predominantly TC1, TH1, and TH17 cells), and innate lymphoid cells recruited from the circulation. These cells and structural cells, including epithelial and endothelial cells and fibroblasts, secrete a variety of proinflammatory mediators, including cytokines, chemokines, growth factors, and lipid mediators. Although most patients with COPD have a predominantly neutrophilic inflammation, some have an increase in eosinophil counts, which might be orchestrated by TH2 cells and type 2 innate lymphoid cells though release of IL-33 from epithelial cells. These patients might be more responsive to corticosteroids and bronchodilators. Oxidative stress plays a key role in driving COPD-related inflammation, even in ex-smokers, and might result in activation of the proinflammatory transcription factor nuclear factor κB (NF-κB), impaired antiprotease defenses, DNA damage, cellular senescence, autoantibody generation, and corticosteroid resistance though inactivation of histone deacetylase 2. Systemic inflammation is also found in patients with COPD and can worsen comorbidities, such as cardiovascular diseases, diabetes, and osteoporosis. Accelerated aging in the lungs of patients with COPD can also generate inflammatory protein release from senescent cells in the lung. In the future, it will be important to recognize phenotypes of patients with optimal responses to more specific therapies, and development of biomarkers that identify the therapeutic phenotypes will be important.

  20. Stance Postural Strategies in Patients with Chronic Inflammatory Demyelinating Polyradiculoneuropathy

    PubMed Central

    Missori, Paolo; Trompetto, Carlo; Fattapposta, Francesco

    2016-01-01

    Introduction Polyneuropathy leads to postural instability and an increased risk of falling. We investigated how impaired motor impairment and proprioceptive input due to neuropathy influences postural strategies. Methods Platformless bisegmental posturography data were recorded in healthy subjects and patients with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). Each subject stood on the floor, wore a head and a hip electromagnetic tracker. Sway amplitude and velocity were recorded and the mean direction difference (MDD) in the velocity vector between trackers was calculated as a flexibility index. Results Head and hip postural sway increased more in patients with CIDP than in healthy controls. MDD values reflecting hip strategies also increased more in patients than in controls. In the eyes closed condition MDD values in healthy subjects decreased but in patients remained unchanged. Discussion Sensori-motor impairment changes the balance between postural strategies that patients adopt to maintain upright quiet stance. Motor impairment leads to hip postural strategy overweight (eyes open), and prevents strategy re-balancing when the sensory context predominantly relies on proprioceptive input (eyes closed). PMID:26977594

  1. Chronic inflammatory demyelinating polyradiculoneuropathy associated with multiple sclerosis.

    PubMed

    Sharma, Khema R; Saadia, Daniela; Facca, Alicia G; Bhatia, Rita; Ayyar, D Ram; Sheremata, William

    2008-06-01

    To describe temporal profile of chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) in patients with definite, relapsing multiple sclerosis (MS). Peripheral demyelinating neuropathy has been rarely reported in association with central nervous system demyelinating disorder indistinguishable from MS. In addition to usual diagnostic studies for CIDP and MS in all 5 patients, we studied proximal segments of nerves using deep tendon reflex latency measurements of biceps reflex, patellar reflex, and ankle reflex. All patients with MS subsequently (4-22 years) developed definite CIDP. Two of these patients developed multiple cranial nerve and spinal root enhancement on subsequent imaging without new intraparenchymal enhancement after a diagnosis of CIDP. The deep tendon reflex latencies were prolonged at more than 2 sites in all patients. Cerebral spinal fluid protein increased (70 +/- 19 to 144.8 +/- 17.4 mg/dL, P = 0.0001) at time of diagnosis of CIDP. Clinical improvement was observed in all patients after intravenous immunoglobulin therapy. When patients with MS develop CIDP, manifestations of central and peripheral disease involvement seem to respond to intravenous immunoglobulin. These cases suggest that there may be common antigenic targets in central and peripheral nervous system in this subset of patients.

  2. Axonal and perikaryal involvement in chronic inflammatory demyelinating polyneuropathy

    PubMed Central

    Nagamatsu, M; Terao, S; Misu, K; Li, M; Hattori, N; Ichimura, M; Sakai, M; Yamamoto, H; Watanabe, H; Riku, S; Ikeda, E; Hata, J; Oda, M; Satake, M; Nakamura, N; Matsuya, S; Hashizume, Y; Sobue, G

    1999-01-01

    OBJECTIVES—To assess the extent of loss of myelinated nerve fibres and spinal motor neuron loss in chronic inflammatory demyelinating polyneuropathy (CIDP), a clinicopathological study was conducted on biopsied sural nerves and necropsied spinal cords from patients with CIDP.
METHODS—The myelinated fibre pathology of 71 biopsied sural nerves and motor neuron pathology of nine necropsied spinal cords at L4 levels in patients with CIDP were quantitatively and immunohistochemically assessed.
RESULTS—Myelinated nerve fibre density was significantly diminished to 65.4% of the control values (p <0.0001), correlating inversely with the extent of segmental demyelination and remyelination (r = −0.43, p < 0.0005) and duration of illness (r = −0.31, p < 0.01). Numbers of large spinal motor neurons in CIDP were variably but significantly diminished (range from 46.0 to 97.6% of the age matched control value (p < 0.005)), and reactive astrogliosis was evident in the ventral horn in CIDP. The frequency of ventral horn neurons exhibiting central chromatolysis and the accumulation of phosphorylated high molecular weight neurofilament protein was significantly higher in CIDP than in controls (p<0.01 and p<0.05).
CONCLUSIONS—The loss of nerve axons and spinal motor neurons is common in CIDP, and extensive in some cases. These neuronal and axonal losses may influence the functional prognosis in CIDP.

 PMID:10329744

  3. Electrophysiological features of POEMS syndrome and chronic inflammatory demyelinating polyneuropathy.

    PubMed

    Guo, Xiuming; Qin, Xinyue; Zhang, Yuping; Huang, Cheng; Yu, Gang

    2014-04-01

    Polyneuropathy is often an initial manifestation of polyneuropathy, organomegaly, endocrinopathy, M protein and skin changes (POEMS) syndrome and therefore this disorder is frequently misdiagnosed as chronic inflammatory demyelinating polyneuropathy (CIDP). We reviewed electrophysiological data in 20 patients with POEMS syndrome and 36 matched patients with CIDP to compare the electrophysiological features of POEMS syndrome and CIDP. Compared with CIDP controls, POEMS patients demonstrated (1) less prolonged distal motor latency and less reduced motor nerve and sensory nerve conduction velocities, (2) greater reduction of amplitudes of compound motor action potentials (CMAP) in distal stimulation, and similar reduction of amplitudes of CMAP in proximal stimulation, (3) similar reduction of amplitudes of sensory nerve action potentials (SNAP) in median and ulnar nerves, and a greater reduction of amplitudes of SNAP in tibial and peroneal nerves, (4) less temporal dispersion, (5) less frequent conduction block, (6) more frequent neurogenic injury in the muscles of the upper and lower limbs, and more frequent neurogenic injury in the muscles of the lower than upper limbs, (7) similar F wave and H reflex abnormalities, and (8) less frequent skin sympathetic response abnormalities. We concluded that before development of typical clinical manifestations, POEMS neuropathy can be distinguished from CIDP by neural electrophysiological examination. These electrophysiological features can be used for early diagnosis and initiating correct treatment of POEMS syndrome.

  4. Chronic renal failure with gout: a marker of chronic lead poisoning

    SciTech Connect

    Craswell, P.W.; Price, J.; Boyle, P.D.; Heazlewood, V.J.; Baddeley, H.; Lloyd, H.M.; Thomas, B.J.; Thomas, B.W.

    1984-09-01

    EDTA (calcium disodium edetate) lead mobilization and x-ray fluorescence (XRF) finger bone lead tests were done in 42 patients with chronic renal failure and without persisting lead intoxication. Nineteen of 23 patients with gout and 8 of 19 without gout had positive EDTA lead mobilization tests. Those patients with gout excreted significantly more excess lead chelate than those without gout. In the gout group 17 patients denied any childhood or industrial exposure to lead. They had a greater number of positive tests and excreted significantly more excess lead chelate than 14 patients with neither gout nor lead exposure. These results confirm that gout in the presence of chronic renal failure is a useful marker of chronic lead poisoning. Of 27 patients with positive lead mobilization tests, only 13 had elevated XRF finger bone lead concentrations (sensitivity 48%). Three of 15 patients with negative lead mobilization tests had elevated XRF finger bone lead concentrations (specificity 80%). Although the XRF finger bone lead test is a convenient noninvasive addition to the diagnostic evaluation of patients with chronic renal failure and gout, its application is limited due to the lack of sensitivity of the method.

  5. Inflammatory milieu as an early marker of kidney injury in offspring rats from diabetic mothers.

    PubMed

    Correa-Costa, Matheus; Landgraf, Maristella A; Cavanal, Maria F; Semedo, Patricia; Vieira, Daniel A G; De Marco, Davi T K; Hirata, Aparecida E; Câmara, Niels O S; Gil, Frida Z

    2012-08-15

    The present study investigated the early presence of inflammatory response in renal tissue of young offspring from diabetic mothers. The effect of L-arginine (L-arg) supplementation was also investigated. The offspring was divided into four groups: group CO (controls); group DO (diabetic offspring); group CA (CO receiving 2% L-arg solution) and group DA (DO receiving the 2% L-arg solution). Glycemia, arterial pressure and renal function were evaluated; gene and protein expression of pro-inflammatory cytokines were also measured. Blood pressure levels were significantly increased in 2 and 6 month-old DO rats, whereas L-arg administration caused a significant decrease in the DA group, at both ages. DO rats showed a significantly blunted glycemic response to exogenous insulin. In 2 month-old DO animals, renal protein expression of pro-inflammatory molecules was significantly increased. At six months of age, we also observed an increase in gene expression of pro-inflammatory molecules, whereas L-arg supplementation prevented this increase at both ages. Our data suggest that activation of inflammatory pathways is present early in the kidney of DO rats, and that L-arg can attenuate the expression of these markers of tissue inflammation. Our results also reinforce the concept that intrauterine environmental factors are a fundamental determinant in the development of metabolic and vascular diseases later in life.

  6. Relationships between Causes of Fever of Unknown Origin and Inflammatory Markers: A Multicenter Collaborative Retrospective Study.

    PubMed

    Naito, Toshio; Torikai, Keito; Mizooka, Masafumi; Mitsumoto, Fujiko; Kanazawa, Kenji; Ohno, Shiro; Morita, Hiroyuki; Ukimura, Akira; Mishima, Nobuhiko; Otsuka, Fumio; Ohyama, Yoshio; Nara, Noriko; Murakami, Kazunari; Mashiba, Kouichi; Akazawa, Kenichiro; Yamamoto, Koji; Tanei, Mika; Yamanouchi, Masashi; Senda, Shoichi; Tazuma, Susumu; Hayashi, Jun

    2015-01-01

    Although inflammatory markers, such as the white blood cell (WBC) count, erythrocyte sedimentation rate (ESR) and levels of C-reactive protein (CRP) and procalcitonin, are widely used to differentiate causes of fever of unknown origin (FUO), little is known about the usefulness of this approach. We evaluated relationships between the causes of classical FUO and the levels of inflammatory markers. A nationwide retrospective study including 17 hospitals affiliated with the Japanese Society of Hospital General Medicine was conducted. This study included 121 patients ≥18 years old diagnosed with "classical FUO" (axillary temperature ≥38.0°C at least twice over a ≥3-week period without elucidation of the cause on three outpatient visits or during three days of hospitalization) between January and December 2011. The causative disease was infectious diseases in 28 patients (23.1%), non-infectious inflammatory disease (NIID) in 37 patients (30.6%), malignancy in 13 patients (10.7%), other in 15 patients (12.4%) and unknown in 28 patients (23.1%). The rate of malignancy was significantly higher for a WBC count of <4,000/μL than for a WBC count of 4,000-8,000/μL (p=0.015). Among the patients with a higher WBC count, the rate of FUO due to NIID tended to be higher and the number of unknown cases tended to be lower. All FUO patients with malignancy showed an ESR of >40 mm/h. A normal ESR appeared to constitute powerful evidence for excluding a diagnosis of malignancy. In contrast, the concentrations of both serum CRP and procalcitonin appeared to be unrelated to the causative disease. The present study identified inflammatory markers that should be considered in the differential diagnosis of classical FUO, providing useful information for future diagnosis.

  7. Inflammatory Markers and Risk of Cerebrovascular Events in Patients Initiating Dialysis

    PubMed Central

    Coresh, Josef; Jaar, Bernard G.; Fink, Nancy E.; Plantinga, Laura C.; Armstrong, Paige A.; Longenecker, J. Craig; Sharrett, A. Richey; Powe, Neil R.; Parekh, Rulan S.

    2011-01-01

    Summary Background and objectives Stroke remains a leading cause of morbidity and mortality for patients on dialysis; however, its risk factors in this population and measures to prevent it are not well understood. Design, setting, participants, & measurements We investigated whether inflammation was associated with cerebrovascular events in a national US cohort of 1041 incident dialysis patients enrolled from October 1995 to June 1998 and followed until January 31, 2004. Incident cerebrovascular events were defined as nonfatal (hospitalized stroke, carotid endarterectomy) and fatal (stroke death) events after dialysis initiation. With Cox proportional hazards regression analysis accounting for the competing risk of nonstroke death, we assessed the independent event risk associated with baseline levels of multiple inflammatory markers (high-sensitivity C-reactive protein [hsCRP], interleukin-6 (IL-6), matrix metalloproteinase-3 [MMP-3], and P-selectin) and hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor (statin) use, which may have pleiotropic inflammatory effects. Results 165 patients experienced a cerebrovascular event during 3548 person-years of follow-up; overall incidence rate was 4.9/100 person-years. None of the inflammatory markers were associated with cerebrovascular event risk (adjusted hazard ratios [HRs] per log unit [95% confidence interval]: hsCRP, 0.97 [0.85 to 1.11]; IL-6, 1.04 [0.85 to 1.26]; MMP-3, 1.02 [0.70 to 1.48]; P-selectin, 0.98 [0.57 to 1.68]). Statin use was also not associated with significant risk of events in unadjusted (HR 1.07 [0.69 to 1.68]) or propensity-score adjusted analyses (HR 0.98 [0.61 to 1.56]). Conclusions In conclusion, neither inflammatory markers nor statin use was associated with risk of cerebrovascular events. Further studies are needed to understand the pathophysiology and prevention of stroke in patients on dialysis. PMID:21551022

  8. Poorer self-rated health is associated with elevated inflammatory markers among older adults.

    PubMed

    Christian, Lisa M; Glaser, Ronald; Porter, Kyle; Malarkey, William B; Beversdorf, David; Kiecolt-Glaser, Janice K

    2011-11-01

    Self-rated health is a strong independent predictor of mortality after accounting for objective health status, behavioral risk factors, and sociodemographic characteristics. However, mechanisms underlying this association are largely unexplained. Inflammation has been associated with increased risk of morbidity and mortality in the elderly. The current study aimed to: (1) examine associations between self-rated health and serum inflammatory markers in older adults; (2) examine the relative strength of these associations for self-rated health versus self-rated change in recent health; (3) examine components of self-rated health that may underlie the association between inflammation and global self-rated health. Self-rated health, as measured by the RAND health survey, and serum interleukin (IL)-6 and C-reactive protein (CRP) were assessed among 250 generally healthy older adults (185 women, 65 men; average age=63.8±13.7 years). A series of linear regression analyses demonstrated that poorer self-rated health was significantly associated with higher IL-6 and CRP. These relationships remained after controlling for age, body mass index, gender, and objective health conditions. These associations also remained after controlling for depressive symptoms, neuroticism, perceived change in health over the past year, and health behaviors (smoking, sleep quality, and physical activity). Analyses of RAND component measures demonstrated that poorer physical functioning was significantly associated with IL-6; the relationship between global self-rated health and both IL-6 and CRP remained after accounting for perceived physical functioning. Poorer self-rated health is associated with elevated serum inflammatory markers among generally healthy older adults. The relationship of self-rated health with inflammatory markers is not secondary to depressive symptoms, neuroticism, or recent changes in perceived health. Subjective ratings of health provide important clinical information

  9. Association of urinary phenolic compounds, inflammatory bowel disease and chronic diarrheal symptoms: Evidence from the National Health and Nutrition Examination Survey.

    PubMed

    de Silva, Punyanganie S; Yang, Xuan; Korzenik, Joshua R; Goldman, Rose H; Arheart, Kristopher L; Caban-Martinez, Alberto J

    2017-10-01

    Endocrine disruptors such as phenolic compounds and parabens may be involved in chronic non-infective disease. While products incorporating these compounds are extensively utilized in consumer and personal products, little is known about their effect on bowel health. Inflammatory bowel disease (IBD) - consisting of the diseases ulcerative colitis and Crohn's disease - and irritable bowel syndrome are common chronic non-infectious diarrheal diseases. Despite limited knowledge on the etiology of IBD, these diseases have increased prevalence in industrialized countries and cause significant impairment to quality of life. In the present study we examine relationships between urinary environmental phenolic compounds, chronic diarrhea and inflammatory bowel disease. Data was obtained from the 2005-2010 US National Health and Nutrition Examination Survey (NHANES) including demographics, lifestyle factors, self-reported health conditions, inflammatory markers and urinary phenolic chemical concentrations. Only participants with complete environmental phenols & parabens component were included in our analysis. Chronic diarrheal symptoms were determined by using the 2009-2010 NHANES questionnaire which included questions pertaining to bowel health. We utilized chronic bowel leakage symptoms as a surrogate marker for chronic diarrhea. The presence of IBD was also analyzed from 2009 to 2010 NHANES data, as a sub-analysis for arthropathy directly querying the presence or absence of IBD. Among the subset of 5218 American adults aged 20-80 years in the NHANES study period who completed environmental phenols & parabens component, 25.5% reported chronic diarrheal symptoms. Abnormal markers of inflammation were present in 2200 (42.2%) of respondents. For IBD, 19 individuals with arthropathy confirmed a diagnosis of ulcerative colitis, and 1 person confirmed a Crohn's diagnosis. After adjustment for demographics, inflammatory and subsample weighing; lower paraben levels were

  10. Peripheral inflammatory markers in Alzheimer's disease: a systematic review and meta-analysis of 175 studies.

    PubMed

    Lai, Ka Sing P; Liu, Celina S; Rau, Allison; Lanctôt, Krista L; Köhler, Cristiano A; Pakosh, Maureen; Carvalho, André F; Herrmann, Nathan

    2017-08-09

    Increasing evidence suggests that inflammation is involved in Alzheimer's disease (AD) pathology. This study quantitatively summarised the data on peripheral inflammatory markers in patients with AD compared with healthy controls (HC). Original reports containing measurements of peripheral inflammatory markers in AD patients and HC were included for meta-analysis. Standardised mean differences were calculated using a random effects model. Meta-regression and exploration of heterogeneity was performed using publication year, age, gender, Mini-Mental State Examination (MMSE) scores, plasma versus serum measurements and immunoassay type. A total of 175 studies were combined to review 51 analytes in 13 344 AD and 12 912 HC patients. Elevated peripheral interleukin (IL)-1β, IL-2, IL-6, IL-18, interferon-γ, homocysteine, high-sensitivity C reactive protein, C-X-C motif chemokine-10, epidermal growth factor, vascular cell adhesion molecule-1, tumour necrosis factor (TNF)-α converting enzyme, soluble TNF receptors 1 and 2, α1-antichymotrypsin and decreased IL-1 receptor antagonist and leptin were found in patients with AD compared with HC. IL-6 levels were inversely correlated with mean MMSE scores. These findings suggest that AD is accompanied by a peripheral inflammatory response and that IL-6 may be a useful biological marker to correlate with the severity of cognitive impairment. Further studies are needed to determine the clinical utility of these markers. © Article author(s) (or their employer(s) unless otherwise stated in the text of the article) 2017. All rights reserved. No commercial use is permitted unless otherwise expressly granted.

  11. Experimental gingivitis induces systemic inflammatory markers in young healthy individuals: a single-subject interventional study.

    PubMed

    Eberhard, Jörg; Grote, Karsten; Luchtefeld, Maren; Heuer, Wieland; Schuett, Harald; Divchev, Dimitar; Scherer, Ralph; Schmitz-Streit, Ruth; Langfeldt, Daniela; Stumpp, Nico; Staufenbiel, Ingmar; Schieffer, Bernhard; Stiesch, Meike

    2013-01-01

    We here investigated whether experimental gingivitis enhances systemic markers of inflammation which are also known as surrogate markers of atherosclerotic plaque development. Gingivitis is a low-level oral infection induced by bacterial deposits with a high prevalence within Western populations. A potential link between the more severe oral disease periodontitis and cardiovascular disease has already been shown. 37 non-smoking young volunteers with no inflammatory disease or any cardiovascular risk factors participated in this single-subject interventional study with an intra-individual control. Intentionally experimental oral inflammation was induced by the interruption of oral hygiene for 21 days, followed by a 21-days resolving phase after reinitiation of oral hygiene. Primary outcome measures at baseline, day 21 and 42 were concentrations of hsCRP, IL-6, and MCP-1, as well as adhesion capacity and oxLDL uptake of isolated blood monocytes. The partial cessation of oral hygiene procedures was followed by the significant increase of gingival bleeding (34.0%, P<0.0001). This local inflammation was associated with a systemic increase in hsCRP (0.24 mg/L, P = 0.038), IL-6 (12.52 ng/L, P = 0.0002) and MCP-1 (9.10 ng/l, P = 0.124) in peripheral blood samples between baseline and day 21, which decreased at day 42. Monocytes showed an enhanced adherence to endothelial cells and increased foam cell formation after oxLDL uptake (P<0.050) at day 21 of gingivitis. Bacterial-induced gingival low-level inflammation induced a systemic increase in inflammatory markers. Dental hygiene almost completely reversed this experimental inflammatory process, suggesting that appropriate dental prophylaxis may also limit systemic markers of inflammation in subjects with natural gingivitis. International Clinical Trials Register Platform of the World Health Organization, registry number: DRKS00003366, URL: http://apps.who.int/trialsearch/Default.aspx.

  12. Advanced oxidation protein product levels as a marker of oxidative stress in paediatric patients with chronic tonsillitis.

    PubMed

    Ozbay, I; Kucur, C; Koçak, F E; Savran, B; Oghan, F

    2016-10-01

    We aimed to determine whether advanced oxidation protein product (AOPP) levels can serve as a marker of oxidative stress in paediatric patients with chronic tonsillitis. Thirty children with chronic tonsillitis and 30 healthy children (control group) were recruited from the Otorhinolaryngology (ORL) and Paediatric Surgery departments, respectively, of Dumlupinar University Hospital. In the patient group, blood samples were collected before tonsillectomy, and tonsil tissue was sampled during the operation. Blood samples were also obtained from the control subjects. AOPP levels in the serum and tonsil tissue were measured by the spectrophotometric method. Serum AOPP levels were significantly higher in the patient group (13.1 ± 3.3 ng/ml) than in the control group (11.6 ± 2.3 ng/ml; P < 0.05). In addition, the mean AOPP level (41.9 ± 13.5 ng/mg protein) in the tonsil tissue in the patient group was significantly higher than the mean serum AOPP levels in the control and patient groups (P < 0.05). AOPP levels are elevated in the tonsil tissue and serum of patients with chronic tonsillitis compared to the serum AOPP levels in healthy controls. AOPPs may represent a novel class of pro-inflammatory molecules that are involved in oxidative stress in chronic tonsillitis. AOPPs may be used as a marker of oxidative stress in paediatric patients with chronic tonsillitis. © Copyright by Società Italiana di Otorinolaringologia e Chirurgia Cervico-Facciale, Rome, Italy.

  13. Peripheral nerve proteins as potential autoantigens in acute and chronic inflammatory demyelinating polyneuropathies.

    PubMed

    Lim, Jia Pei; Devaux, Jérôme; Yuki, Nobuhiro

    2014-10-01

    Guillain-Barré syndrome is classified into acute inflammatory demyelinating polyneuropathy and acute motor axonal neuropathy. Whereas autoantibodies to GM1 or GD1a induce the development of acute motor axonal neuropathy, pathogenic autoantibodies have yet to be identified in acute inflammatory demyelinating polyneuropathy and chronic inflammatory demyelinating polyneuropathy. This review highlights the importance of autoantibodies to peripheral nerve proteins in the physiopathology of acute and chronic inflammatory demyelinating polyneuropathies. Moreover, we listed up other potential antigens, which may become helpful biomarkers for acquired, dysimmune demyelinating neuropathies based on their critical functions during myelination and their implications in hereditary demyelinating neuropathies.

  14. Inflammatory markers are associated with decreased psychomotor speed in patients with major depressive disorder

    PubMed Central

    Goldsmith, David R.; Haroon, Ebrahim; Woolwine, Bobbi J.; Jung, Moon Y.; Wommack, Evanthia C.; Harvey, Philip D.; Treadway, Michael T.; Felger, Jennifer C.; Miller, Andrew H.

    2016-01-01

    Previous data have demonstrated that administration of inflammatory cytokines or their inducers leads to altered basal ganglia function associated with reduced psychomotor speed. Decreased psychomotor speed, referred to clinically as psychomotor retardation, is a cardinal symptom of major depressive disorder (MDD) and has been associated with poor antidepressant treatment response. We therefore examined the association between plasma inflammatory markers and psychomotor speed in ninety-three un-medicated patients with MDD. Psychomotor speed was assessed by a range of neuropsychological tests from purely motor tasks (e.g. movement latency and finger tapping) to those that involved motor activity with increasing cognitive demand and cortical participation (e.g. Trails A and Digit Symbol Substitution Task (DSST)). Linear regression analyses were performed to determine the relationship of inflammatory markers and psychomotor task performance controlling for age, race, sex, education, body mass index, and severity of depression. MDD patients exhibited decreased psychomotor speed on all tasks relative to normative standards. Increased IL-6 was associated with decreased performance on simple and choice movement time tasks, whereas MCP-1 was associated with decreased performance on the finger tapping task and DSST. IL-10 was associated with increased performance on the DSST. In an exploratory principle component analysis including all psychomotor tasks, IL-6 was associated with the psychomotor speed factor. Taken together, the data indicate that a peripheral inflammatory profile including increased IL-6 and MCP-1 is consistently associated with psychomotor speed in MDD. These data are consistent with data demonstrating that inflammation can affect basal ganglia function, and indicate that psychomotor speed may be a viable outcome variable for anti-inflammatory therapies in depression and other neuropsychiatric disorders with increased inflammation. PMID:27040122

  15. SOURCE APPORTIONMENT OF FINE PARTICLES IN THE U.S. AND ASSOCIATIONS BETWEEN INFLAMMATORY MARKER IL -8

    EPA Science Inventory

    Associations are well established between particulate matter (PM) and increased human mortality and morbidity. The association between PM sources and inflammatory marker IL-8 was evaluated in this study.

  16. Chronic low level arsenic exposure evokes inflammatory responses and DNA damage.

    PubMed

    Dutta, Kaustav; Prasad, Priyanka; Sinha, Dona

    2015-08-01

    The cross-sectional study investigated the impact of chronic low level arsenic (As) exposure (11-50μg/L) on CD14 expression and other inflammatory responses in rural women of West Bengal enrolled from control (As level <10μg/L; N, 131) and exposed area (As level 11-50μg/L, N, 142). Atomic absorption spectroscopy revealed that As level in groundwater was higher in endemic areas (22.93±10. 1 vs. 1.61±0.15, P<0.0001) and showed a positive correlation [Pearsons r, 0.9281; 95% confidence interval, 0.8192-0.9724] with As content in nails of the exposed women. Flow cytometric analysis showed that CD 14 expression on monocytes was significantly higher (P<0.001) in exposed women and positively correlated with groundwater As [Pearsons r, 0.9191; 95% confidence interval, 0.7584-0.9745]. Leucocytes and airway cells of As exposed women exhibited up regulation of an inflammatory mediator, tumor necrosis factor-α (TNF-α) and transcription factor, nuclear factor-κB (NF-κB) (P<0.0001). Plasma pro inflammatory cytokines like - TNF-α, interleukins (ILs) - IL-6, IL-8, IL-12 were elevated whereas anti-inflammatory cytokine IL-10 was depleted in the exposed women. Sputa of the exposed women had elevated activity of inflammatory markers - MMP-2 and MMP-9 whereas sera were observed with only increased activity of MMP-9. Airway cells of the exposed women had exacerbated DNA damage than control. Level of oxidative DNA adducts like 8-hydroxy-2'-deoxyguanosine (8OHdG) were also enhanced in plasma of exposed women. Therefore it might be indicated that low level As exposure elicited a pro-inflammatory profile which might have been contributed in part by CD14 expressing monocytes and prolong persistence of pulmonary and systemic inflammation might have promoted oxidative DNA damage in the rural women. Copyright © 2015 Elsevier GmbH. All rights reserved.

  17. Lack of Correlation Between Pulmonary and Systemic Inflammation Markers in Patients with Chronic Obstructive Pulmonary Disease: A Simultaneous, Two-Compartmental Analysis.

    PubMed

    Núñez, Belen; Sauleda, Jaume; Garcia-Aymerich, Judith; Noguera, Aina; Monsó, Eduard; Gómez, Federico; Barreiro, Esther; Marín, Alicia; Antó, Josep Maria; Agusti, Alvar

    2016-07-01

    The origin of systemic inflammation in chronic obstructive pulmonary disease (COPD) patients remains to be defined, but one of the most widely accepted hypothesis is the 'spill over' of inflammatory mediators from the lung to the circulation. To evaluate the relationship between pulmonary and systemic inflammation in COPD quantifying several inflammatory markers in sputum and serum determined simultaneously. Correlations between various inflammatory variables (TNF-α, IL6, IL8) in sputum and serum were evaluated in 133 patients from the PAC-COPD cohort study. A secondary objective was the evaluation of relationships between inflammatory variables and lung function. Inflammatory markers were clearly higher in sputum than in serum. No significant correlation was found (absolute value, r=0.03-0.24) between inflammatory markers in blood and in sputum. There were no significant associations identified between those markers and lung function variables, such as FEV1, DLCO and PaO2 neither. We found no correlation between pulmonary and systemic inflammation in patients with stable COPD, suggesting different pathogenic mechanisms. Copyright © 2016 SEPAR. Published by Elsevier Espana. All rights reserved.

  18. Fibro markers for prediction of hepatocellular carcinoma in egyptian patients with chronic liver disease.

    PubMed

    Mobarak, Lamiaa; Omran, Dalia; Nabeel, Mohammed M; Zakaria, Zeinab

    2016-10-21

    It is well known that hepatocellular carcinoma (HCC) develops as a consequence of hepatic fibrosis progression. In this study, we aimed to evaluate the inflammatory and fibrosis markers as predictors for HCC development among patients with hepatitis C virus (HCV) related chronic liver disease to help in early diagnosis and management of HCC. A total of 280 patients with chronic liver disease were included in this retrospective study, out of them 140 had liver cirrhosis with HCC and 140 had cirrhosis without HCC. Eight readily available blood indices King score, Fibro Q, AST-ALT ratio (AAR), APRI, LOK index, Goteborg University Cirrhosis Index (GUCI), fibro alpha, and Biotechnology Research Center (BRC) were constructed to compare the accuracies of these non invasive scores in predicting HCC development. All fibrosis scores except APRI were significantly higher in HCC. We found that Fibro alpha and BRC had superior diagnostic performance in prediction of HCC based on area under curve of 0.91 and 0.93, respectively compared to other scores with area under curve ranged from poor to failure (0.59-0.66). Almost all cirrhotic cases were secondary to HCV (93.6%), while HBV was detected in 2.1% of cases only. Anti-HCV positive was reported in 100% of HCC cases (P = 0.002). Fibro alpha and BRC scores can be used for prediction of HCC. J. Med. Virol. © 2016 Wiley Periodicals, Inc.

  19. Porphyromonas gingivalis and E. coli Lipopolysaccharide Exhibit Different Systemic but Similar Local Induction of Inflammatory Markers

    PubMed Central

    Liu, Rongkun; Desta, Tesfahun; Raptis, Markos; Darveau, Richard P.; Graves, Dana T.

    2009-01-01

    Background Porphyromonas gingivalis is a gram-negative bacterium that is an important etiologic agent of human adult periodontitis. The goal of the study was to test the hypothesis that two different isoforms, PgLPS1435/1449 and PgLPS1690 exhibit differences in their capacity to stimulate systemic versus local responses compared to E. coli LPS. Methods Lipopolysaccharide (LPS) was inoculated into the scalp of mice and the response was measured locally at the site of site of inoculation and systemically in the heart/aorta. VCAM-1 was assessed at the protein level by ELISA and VCAM-1, E-selectin, and ICAM-1 at the RNA level of RNase protection assay. Serum TNF-α levels were also measured. Results E. coli LPS and both isoforms of P. gingivalis LPS groups were relatively potent in stimulating expression of inflammatory markers with E. coli LPS being somewhat more potent. In contrast, when the systemic response was measured in the heart/aorta, E. coli but not P. gingivalis LPS significantly induced inflammatory markers. At moderate to low doses (1 and 10 ug per injection) serum TNF–α levels were minimally induced by P. gingivalis LPS compared to E. coli LPS. Conclusion The results indicate that both forms of P. gingivalis LPS stimulate an inflammatory response when injected into connective tissue but are minimally stimulatory when a systemic response is measured. In contrast E. coli LPS is a potent stimulus at both the systemic and local level. PMID:18597607

  20. The relationships of current suicidal ideation with inflammatory markers and heart rate variability in unmedicated patients with major depressive disorder.

    PubMed

    Chang, Chuan-Chia; Tzeng, Nian-Sheng; Kao, Yu-Chen; Yeh, Chin-Bin; Chang, Hsin-An

    2017-08-31

    Studies investigating inflammatory status and autonomic functioning simultaneously in depressed patients with current suicidal ideation (SI) are lacking. We recruited 58 unmedicated depressed patients with current SI but without lifetime history of suicidal behavior, as well as 61 equally depressed patients without lifetime history of SI or suicidal behavior. We measured serum cortisol, high-sensitivity C-reactive protein (hs-CRP), erythrocyte sedimentation rate (ESR), and autonomic functioning evaluated by frequency-domain measures of heart rate variability (HRV). The intensity of current SI was rated with the Columbia Suicide Severity Rating Scale. Chronic psychological stress was assessed using the Chinese version of the Perceived Stress Scale (PSS). Patients with current SI showed higher hs-CRP and ESR but lower variance (total HRV), low frequency (LF), and high frequency (HF) HRV than those without lifetime history of SI. We found no differences in cortisol levels and PSS scores. The intensity of current SI was negatively correlated with variance, LF, and HF but positively correlated with hs-CRP. Our results help improve the understanding of the relationships among current SI, inflammation, and autonomic functioning in depressed patients. The combined use of inflammatory markers and HRV indices may one day be applied in predicting and monitoring patients' suicide risk. Copyright © 2017. Published by Elsevier B.V.

  1. Early identification of ‘acute-onset’ chronic inflammatory demyelinating polyneuropathy

    PubMed Central

    Sung, Jia-Ying; Tani, Jowy; Park, Susanna B.; Kiernan, Matthew C.

    2014-01-01

    Distinguishing patients with acute-onset chronic inflammatory demyelinating polyneuropathy from acute inflammatory demyelinating polyneuropathy prior to relapse is often challenging at the onset of their clinical presentation. In the present study, nerve excitability tests were used in conjunction with the clinical phenotype and disease staging, to differentiate between patients with acute-onset chronic inflammatory demyelinating polyneuropathy and patients with acute inflammatory demyelinating polyneuropathy at an early stage, with the aim to better guide treatment. Clinical assessment, staging and nerve excitability tests were undertaken on patients initially fulfilling the diagnostic criteria of acute inflammatory demyelinating polyneuropathy soon after symptom onset and their initial presentation. Patients were subsequently followed up for minimum of 12 months to determine if their clinical presentations were more consistent with acute-onset chronic inflammatory demyelinating polyneuropathy. Clinical severity as evaluated by Medical Research Council sum score and Hughes functional grading scale were not significantly different between the two cohorts. There was no difference between the time of onset of initial symptoms and nerve excitability test assessment between the two cohorts nor were there significant differences in conventional nerve conduction study parameters. However, nerve excitability test profiles obtained from patients with acute inflammatory demyelinating polyneuropathy demonstrated abnormalities in the recovery cycle of excitability, including significantly reduced superexcitability (P < 0.001) and prolonged relative refractory period (P < 0.01), without changes in threshold electrotonus. In contrast, in patients with acute-onset chronic inflammatory demyelinating polyneuropathy, a different pattern occurred with the recovery cycle shifted downward (increased superexcitability, P < 0.05; decreased subexcitability, P < 0.05) and increased

  2. Effects of Synbiotics on Inflammatory Markers in Patients With Type 2 Diabetes Mellitus

    PubMed Central

    Kooshki, A. Akram; Tofighiyan, Tahereh; Rakhshani, Mohamad Hassan

    2015-01-01

    Introduction: With regard to the relationship between inflammation and insulin resistance and due to the lack of researches conducted about the effect of synbiotics on inflammatory markers in diabetes patients, this study was designed to investigate the effect of these markers. Methods: A double-blind, placebo-controlled trial was conducted among 44 type 2 diabetes patients. They were randomized to symbiotic or placebo group. Patients in the symbiotic group received one symbiotic tablet daily for 8 weeks whereas the placebo group received 1 placebo tablet. The hs-CRP concentration, TNF-α and IL-6 were measured by using ELISA kits. The dietary intakes of patients were assessed at the first and the end of the study and analyzed by Nutritionist IV. Data were analyzed by using SPSS 16.0 via paired and independent t- test. Results: Anthropometric and dietary data were not significantly different between the two groups at the first and the end of the study. The serum concentrations of hs-CRP, IL-6 and TNF-α decreased significantly in the symbiotic group at the end of week 8 compared to baseline (p<0.05). Also, no significant changes were seen in the placebo group (p>0.05). The reduction in inflammatory markers in the symbiotic group were significant in compared to the placebo group (P<0.05). Conclusions: Symbiotic supplementation can reduce serum hs-CRP, IL-6 and TNF-α concentrations, a risk factor for cardiovascular diseases. PMID:26153197

  3. Cross Talk between Lipid Metabolism and Inflammatory Markers in Patients with Diabetic Retinopathy.

    PubMed

    Crosby-Nwaobi, Roxanne; Chatziralli, Irini; Sergentanis, Theodoros; Dew, Tracy; Forbes, Angus; Sivaprasad, Sobha

    2015-01-01

    The purpose of this study was to examine the relationship between metabolic and inflammatory markers in patients with diabetic retinopathy (DR). 208 adult patients with type 2 diabetes participated in this study and were categorized into (1) mild nonproliferative diabetic retinopathy (NPDR) without clinically significant macular edema (CSME), (2) NPDR with CSME, (3) proliferative diabetic retinopathy (PDR) without CSME, and (4) PDR with CSME. Variable serum metabolic markers were assessed using immunoassays. Multinomial logistic regression analysis was performed. Diabetes duration and hypertension are the most significant risk factors for DR. Serum Apo-B and Apo-B/Apo-A ratio were the most significant metabolic risk factors for PDR and CSME. For every 0.1 g/L increase in Apo-B concentration, the risk of PDR and CSME increased by about 1.20 times. We also found that 10 pg/mL increase in serum TNF-α was associated with approximately 2-fold risk of PDR/CSME while an increase by 100 pg/mL in serum VEGF concentration correlated with CSME. In conclusion, it seems that there is a link between metabolic and inflammatory markers. Apo-B/Apo-A ratio should be evaluated as a reliable risk factor for PDR and CSME, while the role of increased systemic TNF-α and VEGF should be explored in CSME.

  4. Cross Talk between Lipid Metabolism and Inflammatory Markers in Patients with Diabetic Retinopathy

    PubMed Central

    Crosby-Nwaobi, Roxanne; Chatziralli, Irini; Sergentanis, Theodoros; Dew, Tracy; Forbes, Angus; Sivaprasad, Sobha

    2015-01-01

    Purpose. The purpose of this study was to examine the relationship between metabolic and inflammatory markers in patients with diabetic retinopathy (DR). Methods. 208 adult patients with type 2 diabetes participated in this study and were categorized into (1) mild nonproliferative diabetic retinopathy (NPDR) without clinically significant macular edema (CSME), (2) NPDR with CSME, (3) proliferative diabetic retinopathy (PDR) without CSME, and (4) PDR with CSME. Variable serum metabolic markers were assessed using immunoassays. Multinomial logistic regression analysis was performed. Results. Diabetes duration and hypertension are the most significant risk factors for DR. Serum Apo-B and Apo-B/Apo-A ratio were the most significant metabolic risk factors for PDR and CSME. For every 0.1 g/L increase in Apo-B concentration, the risk of PDR and CSME increased by about 1.20 times. We also found that 10 pg/mL increase in serum TNF-α was associated with approximately 2-fold risk of PDR/CSME while an increase by 100 pg/mL in serum VEGF concentration correlated with CSME. Conclusions. In conclusion, it seems that there is a link between metabolic and inflammatory markers. Apo-B/Apo-A ratio should be evaluated as a reliable risk factor for PDR and CSME, while the role of increased systemic TNF-α and VEGF should be explored in CSME. PMID:26295054

  5. Expression of pericardial fluid T-cells and related inflammatory cytokines in patients with chronic heart failure

    PubMed Central

    Iskandar, Reinard; Liu, Shengchen; Xiang, Fei; Chen, Wen; Li, Liangpeng; Qin, Wei; Huang, Fuhua; Chen, Xin

    2017-01-01

    Pericardial fluid, as a biochemical indicator of heart status, directly indicates pathological alteration to the heart. The accumulation of pericardial fluid can be attributed to an underlying systemic or local inflammatory process. However, the pericardial fluid expression of cellular surface markers, as well as several cytokines in chronic heart failure (CHF), remain unclear. In order to evaluate these issues further the pericardial fluid expression of several cytokines and the surface expression of activity markers between CHF patients and non-heart failure (NHF) patients were analyzed. The pericardial fluid expression of cytokines was measured by immunofluorescence and biomarker of plasma N-terminal propeptide of B-type natriuretic peptide (NT-proBNP), while pericardial fluid levels of soluble glycoprotein 130 (sgp130) were analyzed by ELISA in 50 CHF and 24 NHF patients. In addition, the surface expression of activation markers for T-cells was measured by immunohistochemistry. Patients with CHF demonstrated increased levels of plasma NT-proBNP and pericardial fluid sgp130. Surface expression of cellular activation markers CD25 and Foxp3 in the pericardial fluid was increased in patients with CHF. Moreover, the pro- and anti-inflammatory cytokines interferon (IFN)-γ, interleukin (IL)-6 and IL-10 in patients with CHF also demonstrated an increased expression within its pericardial fluid. In addition, there was infiltration of inflammatory cells and enhanced expression of inflammatory cytokines in the pericardial fluid of patients with CHF, which may reflect T cell activation, suggesting that systemic inflammation is important in the progression of CHF. This evidence could indicate a possible novel target for future therapeutics and prevention of CHF. PMID:28565777

  6. Expression of pericardial fluid T-cells and related inflammatory cytokines in patients with chronic heart failure.

    PubMed

    Iskandar, Reinard; Liu, Shengchen; Xiang, Fei; Chen, Wen; Li, Liangpeng; Qin, Wei; Huang, Fuhua; Chen, Xin

    2017-05-01

    Pericardial fluid, as a biochemical indicator of heart status, directly indicates pathological alteration to the heart. The accumulation of pericardial fluid can be attributed to an underlying systemic or local inflammatory process. However, the pericardial fluid expression of cellular surface markers, as well as several cytokines in chronic heart failure (CHF), remain unclear. In order to evaluate these issues further the pericardial fluid expression of several cytokines and the surface expression of activity markers between CHF patients and non-heart failure (NHF) patients were analyzed. The pericardial fluid expression of cytokines was measured by immunofluorescence and biomarker of plasma N-terminal propeptide of B-type natriuretic peptide (NT-proBNP), while pericardial fluid levels of soluble glycoprotein 130 (sgp130) were analyzed by ELISA in 50 CHF and 24 NHF patients. In addition, the surface expression of activation markers for T-cells was measured by immunohistochemistry. Patients with CHF demonstrated increased levels of plasma NT-proBNP and pericardial fluid sgp130. Surface expression of cellular activation markers CD25 and Foxp3 in the pericardial fluid was increased in patients with CHF. Moreover, the pro- and anti-inflammatory cytokines interferon (IFN)-γ, interleukin (IL)-6 and IL-10 in patients with CHF also demonstrated an increased expression within its pericardial fluid. In addition, there was infiltration of inflammatory cells and enhanced expression of inflammatory cytokines in the pericardial fluid of patients with CHF, which may reflect T cell activation, suggesting that systemic inflammation is important in the progression of CHF. This evidence could indicate a possible novel target for future therapeutics and prevention of CHF.

  7. Efficiency of Double Layered Microencapsulated Probiotic to Modulate ProInflammatory Molecular Markers for the Management of Alcoholic Liver Disease

    PubMed Central

    Kaur, Indu Pal; Chopra, Kanwaljit

    2014-01-01

    Alcohol-related disorders are one of the challenging current health problems with medical, social, and economic consequences. Endotoxemia, oxidative stress, and release of a variety of inflammatory molecules are established mediators in alcoholic liver injury (ALD). Probiotics like L. plantarum though were reported to attenuate ALD, their in vivo health benefits are limited by their survival and sustenance in the adverse gut conditions. Therefore, to enhance their in vivo performance, chitosan coated alginate beads entrapping L. plantarum were prepared, characterized, and evaluated for their efficacy against ALD in rats. Following chronic alcohol exposure, rats developed endotoxemia, showed enhanced levels of liver enzyme markers, NF-κB levels, and increased cytokines such as TNF-α and IL12/p40 subunit, and reflected significant histological changes in the intestine and liver. However, cosupplementation with double layered microencapsulated probiotic significantly (P < 0.05) reduced the levels of endotoxemia, serum transaminases, NF-κB, and cytokines complemented with restoration of normal histoarchitecture of the intestine and liver. It is being documented here for the first time that the probiotics have the potential to inhibit IL-12/p40 subunit which is a recently explored potential marker for developing novel therapeutic agents. This study reveals that microencapsulation of probiotics may offer a biopharmacological basis for effective management of ALD. PMID:24966470

  8. Association between Serum Neopterin and Inflammatory Activation in Chronic Kidney Disease

    PubMed Central

    Yadav, Ashok Kumar; Sharma, Vinod; Jha, Vivekanand

    2012-01-01

    Background. The serum levels of neopterin, a marker associated with cell-mediated immunity are elevated in chronic kidney disease (CKD). We evaluated serum neopterin levels and investigated its association with markers of inflammation in a cross-section of CKD subjects without known cardiovascular disease. Methods. Serum neopterin levels were measured in 118 patients with stage 3–5 CKD and 41 healthy subjects with normal kidney function (HC). Patients with known cardiovascular disease were excluded. We also estimated highly sensitive CRP (hsCRP) and interluekin-6 (IL-6), tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ) in the CKD subjects. All assays were done using commercially available ELISA kits. The correlation between neopterin and markers of inflammation were investigated. Results. Of the CKD population, 82 were in stage 5 (60 stage 5 D), 24 in stage 4, and 12 in stage 3. The mean age was 51.04 ± 1.3 years and 66% were males. The commonest cause of CKD was diabetes (36%). Serum neopterin levels were 5-fold higher in CKD patients as compared to HC (74.8 ± 3.6 versus 15.0 ± 2.8 nmol/L, P < 0.0001). There was a graded increase of serum neopterin from stages 3 to 4 and 5. CKD 5 D patients exhibited significantly higher levels compared to nondialysis stage 5 patients (P < 0.0001). An inverse correlation was noted between serum neopterin and eGFR (r = −0.359, P < 0.0001). Serum neopterin correlated with hsCRP (r = 0.285, P = 0.002), IL-6 (r = 0.212, P = 0.034), and IFN-γ (r = 0.32, P = 0.001) but not with TNF-α. Conclusion. Serum neopterin level is elevated and correlates with the severity of CKD. The elevation correlates with elevation of most, but not all, inflammatory markers. Its role in future development of cardiovascular disease and modulation with anti-inflammatory therapies needs further studies. PMID:22969169

  9. Association between serum neopterin and inflammatory activation in chronic kidney disease.

    PubMed

    Yadav, Ashok Kumar; Sharma, Vinod; Jha, Vivekanand

    2012-01-01

    The serum levels of neopterin, a marker associated with cell-mediated immunity are elevated in chronic kidney disease (CKD). We evaluated serum neopterin levels and investigated its association with markers of inflammation in a cross-section of CKD subjects without known cardiovascular disease. Serum neopterin levels were measured in 118 patients with stage 3-5 CKD and 41 healthy subjects with normal kidney function (HC). Patients with known cardiovascular disease were excluded. We also estimated highly sensitive CRP (hsCRP) and interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ) in the CKD subjects. All assays were done using commercially available ELISA kits. The correlation between neopterin and markers of inflammation were investigated. Of the CKD population, 82 were in stage 5 (60 stage 5 D), 24 in stage 4, and 12 in stage 3. The mean age was 51.04 ± 1.3 years and 66% were males. The commonest cause of CKD was diabetes (36%). Serum neopterin levels were 5-fold higher in CKD patients as compared to HC (74.8 ± 3.6 versus 15.0 ± 2.8 nmol/L, P < 0.0001). There was a graded increase of serum neopterin from stages 3 to 4 and 5. CKD 5 D patients exhibited significantly higher levels compared to nondialysis stage 5 patients (P < 0.0001). An inverse correlation was noted between serum neopterin and eGFR (r = -0.359, P < 0.0001). Serum neopterin correlated with hsCRP (r = 0.285, P = 0.002), IL-6 (r = 0.212, P = 0.034), and IFN-γ (r = 0.32, P = 0.001) but not with TNF-α. Serum neopterin level is elevated and correlates with the severity of CKD. The elevation correlates with elevation of most, but not all, inflammatory markers. Its role in future development of cardiovascular disease and modulation with anti-inflammatory therapies needs further studies.

  10. Chronic intestinal inflammation: inflammatory bowel disease and colitis-associated colon cancer

    PubMed Central

    Rubin, Deborah C.; Shaker, Anisa; Levin, Marc S.

    2012-01-01

    The inflammatory bowel diseases (IBD), including Crohn’s disease (CD) and ulcerative colitis (UC), are chronic inflammatory disorders of the intestine. The prevalence in the United States is greater than 200 cases per 100,000, with the total number of IBD patients between 1 and 1.5 million. CD may affect all parts of the gastrointestinal tract, from mouth to anus, but most commonly involves the distal part of the small intestine or ileum, and colon. UC results in colonic inflammation that can affect the rectum only, or can progress proximally to involve part of or the entire colon. Clinical symptoms include diarrhea, abdominal pain, gastrointestinal bleeding, and weight loss. A serious long-term complication of chronic inflammation is the development of colorectal cancer. A genetic basis for IBD had long been recognized based on the increased familial risk. However, significant discordance for CD in twins, and a much less robust phenotypic concordance for UC, suggested additional factors play a role in disease pathogenesis, including environmental factors. In the past several years, progress in understanding the molecular basis of IBD has accelerated, beginning with the generation of animal models of colitis and progressing to the identification of specific genetic markers from candidate gene, gene linkage, and genome-wide association analyses. Genetic studies have also resulted in the recognition of the importance of environmental factors, particularly the crucial role of the gut microbiota in CD and UC. Altered immune responses to the normal intestinal flora are key factors in IBD pathogenesis. In this research topic, the genetic basis of IBD, the genetic and cellular alterations associated with colitis-associated colon cancer, and the emerging role of the intestinal microbiota and other environmental factors will be reviewed. PMID:22586430

  11. Cinnamon extract reduces symptoms, inflammatory mediators and mast cell markers in murine IL-10(-/-) colitis.

    PubMed

    Hagenlocher, Yvonne; Hösel, Angela; Bischoff, Stephan C; Lorentz, Axel

    2016-04-01

    Inflammatory bowel disease (IBD) shows an increasing prevalence and harm in western countries. Conventional therapies are associated with bad compliance and adverse side effects. Natural substances like cinnamon extract (CE) could be an additional therapy. We found recently that CE acts anti-inflammatory on mast cells - discussed of being relevant in IBD. Here, we analysed the effects of CE on murine IL-10(-/-) colitis as model for IBD. Mice were treated 12 weeks with or without CE in drinking water. Clinical scores and disease activity index were assessed. Colonic tissue samples were analysed for infiltration, tissue damage, bowel wall thickness, expression of pro-inflammatory mediators, mast cell proteases, tight junction proteins, and NF-κB signaling. Following treatment with CE, symptoms of murine colitis as well as increased infiltration of immune cells, tissue damage and bowel wall thickness in colon tissue of IL-10(-/-) mice were diminished significantly. MIP-2, TNF, IFNγ, CCL2, CCL3, CCL4 and IL-1β as well as MC-CPA, MCP-1 and MCP-4 were strongly upregulated in IL-10(-/-) mice compared to WT, but noteworthy not in CE group. Expression of tight junction proteins was not influenced by CE. Phosphorylation of IκB was slightly down-regulated in CE treated IL-10(-/-) mice compared to IL-10(-/-) controls. In summary, CE decreases inflammatory symptoms and expression of inflammatory markers in murine IL-10(-/-) colitis. CE has no influence on tight junction proteins, but seems acting via reducing pro-inflammatory mediators and recruitment of neutrophil granulocytes probably by inhibiting NF-κB signaling. Copyright © 2015 Elsevier Inc. All rights reserved.

  12. Time From Smoking Cessation and Inflammatory Markers: New Evidence From a Cross-Sectional Analysis of ELSA-Brasil.

    PubMed

    Peres, Flávia Soares; Barreto, Sandhi Maria; Camelo, Lidyane V; Ribeiro, Antonio Luiz P; Vidigal, Pedro Guatimosim; Duncan, Bruce Bartholow; Giatti, Luana

    2017-07-01

    The time for inflammatory markers of former smokers to revert to never smoker levels is still controversial, ranging from 5 to 20 years. We aimed to determine the time from smoking cessation for white blood cell (WBC) count and serum C-reactive protein (CRP) levels to return to those of never-smokers, after adjusting for confounding factors and for secondhand smoke (SHS) exposure among participants of the Brazilian Longitudinal Study of Adult Health (ELSA-Brasil). Cross-sectional analysis of baseline participants of ELSA-Brasil. We used linear regression analysis and generalized linear models with gamma distribution and logarithmic link function to estimate the association of WBC count and CRP levels with time from smoking cessation. The following confounding factors were considered: sex, age, education, SHS, alcohol consumption, leisure-time physical activity, BMI, total cholesterol/HDL ratio, hypertension, diabetes, cardiovascular disease, and chronic obstructive pulmonary disease (COPD). Results: After all adjustments, time from smoking cessation <10 years remained associated with higher WBC count (eg, time from smoking cessation ≥ 5 and <10 years: β: 167.92; 95%CI: 23.52 312.31), while only time from smoking cessation <1 year remained associated with higher arithmetic mean of CRP (AMR: 1.26, 95%CI: 1.03‒1.54). Levels of inflammatory markers were similar to those of never-smokers 1 year after smoking cessation for CRP and 10 years after for WBC. The results may add to the arsenal health professionals have to encourage their patients to quit smoking, as some harms from smoking appear to revert to never-smokers' level sooner than previously reported. Longitudinal studies should confirm our findings.

  13. Surveys on therapeutic effects of “halotherapy chamber with artificial salt-mine environment” on patients with certain chronic allergenic respiratory pathologies and infectious-inflammatory pathologies

    PubMed Central

    Lazarescu, H; Simionca, I; Hoteteu, M; Munteanu, A; Rizea, I; Iliuta, A; Dumitrascu, D; Dumitrescu, E

    2014-01-01

    Halotherapy (HT), derived from speleotherapy in salt mines, is also a drug-free therapeutic method. HT effects vary depending on the therapeutic method and the structure of halotherapy environment. The purpose of this article is to show the HT effects of “halotherapy chamber with artificial salt-mine environment” of the National Institute of Rehabilitation, Physical Medicine and Balneoclimatology (INRMFB), on patients with bronchial asthma and other chronic, infectious-inflammatory and allergic respiratory diseases, describing the clinical effects on certain nonspecific resistance factors, on markers of inflammatory processes and on certain immunological changes. Patients were clinically assessed, with the application of hematologic investigations, analysis of nonspecific resistance to infection and of inflammatory process markers, immunologic assessments, analysis of sodium and potassium concentrations, of mineralocorticoid function and other biochemical tests. For the experimental HT therapy performed in the “halotherapy chamber with artificial salt-mine environment” of INRMFB, 15 patients suffering from bronchial asthma, allergic rhinitis, chronic bronchitis, chronic obstructive bronchopneumopathy were selected, based on specific medical indications and contraindications and applying ethical principles, as well as 4 patients with similar pathologies for the control group, who underwent in-home drug treatment. After the specific halotherapy treatment on patients with bronchial asthma, chronic bronchitis and chronic obstructive bronchopneumopathy, which also showed other chronic, infectious-inflammatory and allergic respiratory pathologies, triggering of anti-inflammatory (and also anti allergic) mechanisms and healing effects on inflammatory process were noted. Data acquired also proved the halo therapeutic effect causing the reduction of sensitiveness of body in patients with bronchial asthma. Abbreviations: HT=Halotherapy, INRMFB=National Institute of

  14. Surveys on therapeutic effects of "halotherapy chamber with artificial salt-mine environment" on patients with certain chronic allergenic respiratory pathologies and infectious-inflammatory pathologies.

    PubMed

    Lazarescu, H; Simionca, I; Hoteteu, M; Munteanu, A; Rizea, I; Iliuta, A; Dumitrascu, D; Dumitrescu, E

    2014-01-01

    Halotherapy (HT), derived from speleotherapy in salt mines, is also a drug-free therapeutic method. HT effects vary depending on the therapeutic method and the structure of halotherapy environment. The purpose of this article is to show the HT effects of "halotherapy chamber with artificial salt-mine environment" of the National Institute of Rehabilitation, Physical Medicine and Balneoclimatology (INRMFB), on patients with bronchial asthma and other chronic, infectious-inflammatory and allergic respiratory diseases, describing the clinical effects on certain nonspecific resistance factors, on markers of inflammatory processes and on certain immunological changes. Patients were clinically assessed, with the application of hematologic investigations, analysis of nonspecific resistance to infection and of inflammatory process markers, immunologic assessments, analysis of sodium and potassium concentrations, of mineralocorticoid function and other biochemical tests. For the experimental HT therapy performed in the "halotherapy chamber with artificial salt-mine environment" of INRMFB, 15 patients suffering from bronchial asthma, allergic rhinitis, chronic bronchitis, chronic obstructive bronchopneumopathy were selected, based on specific medical indications and contraindications and applying ethical principles, as well as 4 patients with similar pathologies for the control group, who underwent in-home drug treatment. After the specific halotherapy treatment on patients with bronchial asthma, chronic bronchitis and chronic obstructive bronchopneumopathy, which also showed other chronic, infectious-inflammatory and allergic respiratory pathologies, triggering of anti-inflammatory (and also anti allergic) mechanisms and healing effects on inflammatory process were noted. Data acquired also proved the halo therapeutic effect causing the reduction of sensitiveness of body in patients with bronchial asthma.

  15. Childhood chronic inflammatory demyelinating polyneuropathy: an overview of 10 cases in the modern era.

    PubMed

    Ware, Tyson L; Kornberg, Andrew J; Rodriguez-Casero, M Victoria; Ryan, Monique M

    2014-01-01

    Chronic inflammatory demyelinating polyneuropathy is a rare condition in children. In this article, we report our experience in the management of 10 cases of childhood chronic inflammatory demyelinating polyneuropathy in a single center, in the era of contrast-enhanced magnetic resonance imaging (MRI), genetic microarray, and chronic inflammatory demyelinating polyneuropathy disease activity status. Robust neurophysiologic abnormalities were present in all cases and both MRI and lumbar puncture were useful adjuncts in diagnosis. Genetic microarray is a simple technique useful in excluding the most common hereditary demyelinating neuropathy. Intravenous immunoglobulin was an effective first-line therapy in most cases, with refractory cases responding to corticosteroids and rituximab. We found the chronic inflammatory demyelinating polyneuropathy disease activity status useful for assessing outcome at final follow-up, whereas the modified Rankin score was better for assessing peak motor disability.

  16. To assess, to control, to exclude: Effects of biobehavioral factors on circulating inflammatory markers

    PubMed Central

    O’Connor, Mary-Frances; Bower, Julie E.; Cho, Hyong Jin; Creswell, J. David; Dimitrov, Stoyan; Hamby, Mary E.; Hoyt, Michael A.; Martin, Jennifer L.; Robles, Theodore F.; Sloan, Erica K.; Thomas, KaMala S.; Irwin, Michael R.

    2009-01-01

    Behavioral scientists have increasingly included inflammatory biology as mechanisms in their investigation of psychosocial dynamics on the pathobiology of disease. However, a lack of standardization of inclusion and exclusion criteria and assessment of relevant control variables impacts the interpretation of these studies. The present paper reviews and discusses human biobehavioral factors that can affect the measurement of circulating markers of inflammation. Keywords relevant to inflammatory biology and biobehavioral factors were searched through PubMed. Age, sex, and hormonal status, socioeconomic status, ethnicity and race, body mass index, exercise, diet, caffeine, smoking, alcohol, sleep disruption, antidepressants, aspirin, and medications for cardiovascular disease are all reviewed. A tiered set of recommendations as to whether each variable should be assessed, controlled for, or used as an exclusion criteria is provided. These recommendations provide a framework for observational and intervention studies investigating linkages between psychosocial and behavioral factors and inflammation. PMID:19389469

  17. To assess, to control, to exclude: effects of biobehavioral factors on circulating inflammatory markers.

    PubMed

    O'Connor, Mary-Frances; Bower, Julie E; Cho, Hyong Jin; Creswell, J David; Dimitrov, Stoyan; Hamby, Mary E; Hoyt, Michael A; Martin, Jennifer L; Robles, Theodore F; Sloan, Erica K; Thomas, Kamala S; Irwin, Michael R

    2009-10-01

    Behavioral scientists have increasingly included inflammatory biology as mechanisms in their investigation of psychosocial dynamics on the pathobiology of disease. However, a lack of standardization of inclusion and exclusion criteria and assessment of relevant control variables impacts the interpretation of these studies. The present paper reviews and discusses human biobehavioral factors that can affect the measurement of circulating markers of inflammation. Keywords relevant to inflammatory biology and biobehavioral factors were searched through PubMed. Age, sex, and hormonal status, socioeconomic status, ethnicity and race, body mass index, exercise, diet, caffeine, smoking, alcohol, sleep disruption, antidepressants, aspirin, and medications for cardiovascular disease are all reviewed. A tiered set of recommendations as to whether each variable should be assessed, controlled for, or used as an exclusion criteria is provided. These recommendations provide a framework for observational and intervention studies investigating linkages between psychosocial and behavioral factors and inflammation.

  18. Genome sequencing elucidates Sardinian genetic architecture and augments association analyses for lipid and blood inflammatory markers

    PubMed Central

    Zoledziewska, Magdalena; Mulas, Antonella; Pistis, Giorgio; Steri, Maristella; Danjou, Fabrice; Kwong, Alan; Ortega del Vecchyo, Vicente Diego; Chiang, Charleston W. K.; Bragg-Gresham, Jennifer; Pitzalis, Maristella; Nagaraja, Ramaiah; Tarrier, Brendan; Brennan, Christine; Uzzau, Sergio; Fuchsberger, Christian; Atzeni, Rossano; Reinier, Frederic; Berutti, Riccardo; Huang, Jie; Timpson, Nicholas J; Toniolo, Daniela; Gasparini, Paolo; Malerba, Giovanni; Dedoussis, George; Zeggini, Eleftheria; Soranzo, Nicole; Jones, Chris; Lyons, Robert; Angius, Andrea; Kang, Hyun M.; Novembre, John; Sanna, Serena; Schlessinger, David; Cucca, Francesco; Abecasis, Gonçalo R

    2015-01-01

    We report ~17.6M genetic variants from whole-genome sequencing of 2,120 Sardinians; 22% are absent from prior sequencing-based compilations and enriched for predicted functional consequence. Furthermore, ~76K variants common in our sample (frequency >5%) are rare elsewhere (<0.5% in the 1000 Genomes Project). We assessed the impact of these variants on circulating lipid levels and five inflammatory biomarkers. Fourteen signals, including two major new loci, were observed for lipid levels, and 19, including two novel loci, for inflammatory markers. New associations would be missed in analyses based on 1000 Genomes data, underlining the advantages of large-scale sequencing in this founder population. PMID:26366554

  19. Pathophysiological mechanisms of acute pancreatitis define inflammatory markers of clinical prognosis.

    PubMed

    Minkov, Georgi A; Halacheva, Krasimira S; Yovtchev, Yovcho P; Gulubova, Maya V

    2015-07-01

    Development of acute pancreatitis illustrates the need to understand the basic mechanisms of disease progression to drive the exploration of therapeutic options. Cytokines play a major role in the pathogenesis of acute pancreatitis as underlying systemic inflammatory response, tissue damage, and organ dysfunction. However, little is known about circulating concentrations of these inflammatory markers and their real impact on clinical practice. Experimental studies have suggested that the prognosis for acute pancreatitis depends on the degree of pancreatic necrosis and the intensity of multisystem organ failure generated by the systemic inflammatory response. This suggests an intricate balance between localized tissue damage with proinflammatory cytokine production and a systemic anti-inflammatory response that restricts the inappropriate movement of proinflammatory agents into the circulation. Implication of such mediators suggests that interruption or blunting of an inappropriate immune response has the potential to improve outcome. A detailed understanding of pathophysiological processes and immunological aspects in patients with acute pancreatitis is the basis for the development of therapeutic strategies that will provide significant reductions in morbidity and mortality.

  20. Serum inflammatory markers in overweight children and adolescents with non-alcoholic fatty liver disease.

    PubMed

    Neuman, Gal; Sagi, Rami; Shalitin, Shlomit; Reif, Shimon

    2010-07-01

    Obesity, a worldwide pandemia, is associated with a large variety of comorbidities, among which is non-alcoholic fatty liver disease. NAFLD is a complex disease that may eventually lead to cirrhosis, posing a high risk for the patient and thus necessitating early diagnosis and treatment. To evaluate the association between ultrasonographically diagnosed non-alcoholic fatty liver disease and the levels of serum inflammatory markers in obese children and adolescents. This prospective cohort study was conducted in children and adolescents attending the endocrine obesity clinic in a tertiary care children's hospital in 2001-2003. Blood tests and ultrasound were performed to detect the presence of fatty liver. The severity of fatty liver was determined by measuring the liver/kidney echogenicity ratio (hepatorenal index). Blood tests included complete blood count, liver enzymes, lipid profile, erythrocyte sedimentation rate, high sensitivity C-reactive protein, serum amyloid A, and the degree of erythrocyte adhesiveness/aggregation as measured in peripheral blood slides. The 30 boys and 34 girls, age 9-21 years, who participated in the study were divided into those who evidenced NAFLD on ultrasound (Group 1, n=37) and those whose liver appeared normal on ultrasound (Group 2, n=24). ESR, hs-CRP, SAA and the degree of erythrocyte adhesiveness/aggregation were compared between the groups. There was no significant association between elevated ESR, the levels of CRP, SAA and/or the degree of erythrocyte adhesiveness/aggregation and the hepatorenal index and NAFLD. The degree of erythrocyte adhesiveness/ aggregation correlated with body mass index-standard deviation score in both genders (P < 0.05). Fatty liver itself may not be a cofactor in stimulating inflammatory markers in obese patients. Obese children diagnosed with NAFLD may have simple steatosis and their increased inflammatory markers are therefore compatible with those expected in obesity.

  1. Inflammatory Markers in Blood and Exhaled Air after Short-Term Exposure to Cooking Fumes

    PubMed Central

    Svedahl, Sindre Rabben

    2013-01-01

    Objectives: Cooking fumes contain aldehydes, alkanoic acids, polycyclic aromatic hydrocarbons, and heterocyclic compounds. The inhalation of cooking fumes entails a risk of deleterious health effects. The aim of this study was to see if the inhalation of cooking fumes alters the expression of inflammatory reactions in the bronchial mucosa and its subsequent systemic inflammatory response in blood biomarkers. Methods: Twenty-four healthy volunteers stayed in a model kitchen on two different occasions for 2 or 4h. On the first occasion, there was only exposure to normal air, and on the second, there was exposure to controlled levels of cooking fumes. On each occasion, samples of blood, exhaled air, and exhaled breath condensate (EBC) were taken three times in 24h and inflammatory markers were measured from all samples. Results: There was an increase in the concentration of the d-dimer in blood from 0.27 to 0.28mg ml–1 on the morning after exposure to cooking fumes compared with the levels the morning before (P-value = 0.004). There was also a trend of an increase in interleukin (IL)-6 in blood, ethane in exhaled air, and IL-1β in EBC after exposure to cooking fumes. In a sub-analysis of 12 subjects, there was also an increase in the levels of ethane—from 2.83 parts per billion (ppb) on the morning before exposure to cooking fumes to 3.53 ppb on the morning after exposure (P = 0.013)—and IL-1β—from 1.04 on the morning before exposure to cooking fumes to 1.39 pg ml–1 immediately after (P = 0.024). Conclusion: In our experimental setting, we were able to unveil only small changes in the levels of inflammatory markers in exhaled air and in blood after short-term exposure to moderate concentrations of cooking fumes. PMID:23179989

  2. The outcome of short-term low-dose aspirin treatment in Kawasaki disease based on inflammatory markers

    PubMed Central

    Yoo, Jae Won; Kim, Ji Mok

    2017-01-01

    Purpose Previously, Kawasaki disease (KD) treatment with low-dose aspirin was administered for 6–8 weeks after the acute phase. However, inflammatory marker levels normalize before 6–8 weeks. In this study, we aimed to investigate the clinical outcome of short-term low-dose aspirin treatment based on inflammatory and thrombotic marker levels. Methods We performed a retrospective review of the medical records of patients with KD who were hospitalized at Chungnam National University Hospital between September 2012 and May 2014. When fever subsided, low-dose aspirin treatment was started. Inflammatory (white blood cell count, erythrocyte sedimentation rate, and C-reactive protein) and thrombotic markers (D-dimer) were monitored at follow-ups conducted in 1- to 2-week intervals. The low-dose aspirin administration was terminated when both markers were normalized and no cardiovascular complications were observed. Results Eighty-four patients with KD (complete KD, n=49; incomplete KD, n=35) were enrolled. The inflammatory and thrombotic marker levels were normalized within 3–4 weeks on average. At the beginning the low-dose aspirin treatment, 9 patients had coronary artery lesions but 75 did not. When the low-dose aspirin administration was terminated at the time the inflammatory marker levels were normalized, no new CALs developed during the follow-up at 6–8 weeks. Conclusion Most of the inflammatory marker levels were normalized within 3–4 weeks after the acute phase of KD. New cardiovascular complications did not develop during the course of the short-term aspirin treatment based on the inflammatory marker levels, clinical findings, and echocardiography. PMID:28203257

  3. The outcome of short-term low-dose aspirin treatment in Kawasaki disease based on inflammatory markers.

    PubMed

    Yoo, Jae Won; Kim, Ji Mok; Kil, Hong Ryang

    2017-01-01

    Previously, Kawasaki disease (KD) treatment with low-dose aspirin was administered for 6-8 weeks after the acute phase. However, inflammatory marker levels normalize before 6-8 weeks. In this study, we aimed to investigate the clinical outcome of short-term low-dose aspirin treatment based on inflammatory and thrombotic marker levels. We performed a retrospective review of the medical records of patients with KD who were hospitalized at Chungnam National University Hospital between September 2012 and May 2014. When fever subsided, low-dose aspirin treatment was started. Inflammatory (white blood cell count, erythrocyte sedimentation rate, and C-reactive protein) and thrombotic markers (D-dimer) were monitored at follow-ups conducted in 1- to 2-week intervals. The low-dose aspirin administration was terminated when both markers were normalized and no cardiovascular complications were observed. Eighty-four patients with KD (complete KD, n=49; incomplete KD, n=35) were enrolled. The inflammatory and thrombotic marker levels were normalized within 3-4 weeks on average. At the beginning the low-dose aspirin treatment, 9 patients had coronary artery lesions but 75 did not. When the low-dose aspirin administration was terminated at the time the inflammatory marker levels were normalized, no new CALs developed during the follow-up at 6-8 weeks. Most of the inflammatory marker levels were normalized within 3-4 weeks after the acute phase of KD. New cardiovascular complications did not develop during the course of the short-term aspirin treatment based on the inflammatory marker levels, clinical findings, and echocardiography.

  4. Are faecal markers good indicators of mucosal healing in inflammatory bowel disease?

    PubMed Central

    Boon, Gudula JAM; Day, Andrew S; Mulder, Chris J; Gearry, Richard B

    2015-01-01

    AIM: To review the published literature concerning the accuracy of faecal inflammatory markers for identifying mucosal healing. METHODS: Bibliographical searches were performed in MEDLINE electronic database up to February 2015, using the following terms: “inflammatory bowel disease”, “Crohn´s disease”, “ulcerative colitis”, “faecal markers”, “calprotectin”, “lactoferrin”, “S100A12”, “endoscop*”, “mucosal healing”, “remission”. In addition, relevant references from these studies were also included. Data were extracted from the published papers including odds ratios with 95%CI, P values and correlation coefficients. Data were grouped together according to each faecal marker, Crohn’s disease or ulcerative colitis, and paediatric compared with adult study populations. Studies included in this review assessed mucosal inflammation by endoscopic and/or histological means and compared these findings to faecal marker concentrations in inflammatory bowel diseases (IBD) patient cohorts. Articles had to be published between 1990 and February 2015 and written in English. Papers excluded from the review were those where the faecal biomarker concentration was compared between patients with IBD and controls or other disease groups, those where serum biomarkers were used, those with a heterogeneous study population and those only assessing post-operative disease. RESULTS: The available studies show that faecal markers, such as calprotectin and lactoferrin, are promising non-invasive indicators of mucosal healing. However, due to wide variability in study design, especially with regard to the definition of mucosal healing and evaluation of marker cut offs, the available data do not yet indicate the optimal roles of these markers. Thirty-six studies published between 1990 and 2014 were included. Studies comprised variable numbers of study participants, considered CD (15-164 participants) or UC (12-152 participants) separately or as a

  5. An animal model of chronic inflammatory pain: pharmacological and temporal differentiation from acute models.

    PubMed

    Wilson, Alex W; Medhurst, Stephen J; Dixon, Claire I; Bontoft, Nick C; Winyard, Lisa A; Brackenborough, Kim T; De Alba, Jorge; Clarke, Christopher J; Gunthorpe, Martin J; Hicks, Gareth A; Bountra, Chas; McQueen, Daniel S; Chessell, Iain P

    2006-08-01

    Clinically, inflammatory pain is far more persistent than that typically modelled pre-clinically, with the majority of animal models focussing on short-term effects of the inflammatory pain response. The large attrition rate of compounds in the clinic which show pre-clinical efficacy suggests the need for novel models of, or approaches to, chronic inflammatory pain if novel mechanisms are to make it to the market. A model in which a more chronic inflammatory hypersensitivity phenotype is profiled may allow for a more clinically predictive tool. The aims of these studies were to characterise and validate a chronic model of inflammatory pain. We have shown that injection of a large volume of adjuvant to the intra-articular space of the rat knee results in a prolonged inflammatory pain response, compared to the response in an acute adjuvant model. Additionally, this model also results in a hypersensitive state in the presence and absence of inflammation. A range of clinically effective analgesics demonstrate activity in this chronic model, including morphine (3mg/kg, t.i.d.), dexamethasone (1mg/kg, b.i.d.), ibuprofen (30mg/kg, t.i.d.), etoricoxib (5mg/kg, b.i.d.) and rofecoxib (0.3-10mg/kg, b.i.d.). A further aim was to exemplify the utility of this chronic model over the more acute intra-plantar adjuvant model using two novel therapeutic approaches; NR2B selective NMDA receptor antagonism and iNOS inhibition. Our data shows that different effects were observed with these therapies when comparing the acute model with the model of chronic inflammatory joint pain. These data suggest that the chronic model may be more relevant to identifying mechanisms for the treatment of chronic inflammatory pain states in the clinic.

  6. Chronic inflammatory appendiceal conditions that mimic acute appendicitis on helical CT.

    PubMed

    Checkoff, Jaime L; Wechsler, Richard J; Nazarian, Levon N

    2002-09-01

    Acute appendicitis is commonly diagnosed on CT, but chronic appendiceal processes can mimic acute appendicitis. The purpose of this study was to identify the frequency of these alternative conditions and their findings on helical CT. Chronic inflammatory conditions other than acute appendicitis were found in 9% of patients who underwent surgery after CT findings were interpreted as suspicious for appendicitis. These inflammatory conditions were indistinguishable from acute appendicitis when we used either primary or secondary CT signs.

  7. Interleukins and inflammatory markers in in-stent restenosis after femoral percutaneous transluminal angioplasty.

    PubMed

    Araújo, Paula Vasconcelos; Ribeiro, Maurício Serra; Dalio, Marcelo Bellini; Rocha, Laura Andrade; Viaro, Fernanda; Dellalibera Joviliano, Renata; Piccinato, Carlos Eli; Évora, Paulo Roberto Barbosa; Joviliano, Edwaldo Edner

    2015-01-01

    Inflammatory activity may influence results of percutaneous transluminal angioplasty (PTA). The purpose of this study was to evaluate the relationship between (1) proinflammatory markers (interleukin [IL]-6, IL-8, tumor necrosis factor α (TNF-α), and highly sensitive C-reactive protein [CRP]); (2) type 1 T helper cell marker (IL-12); and (3) Type 2 T helper cell marker (transforming growth factor-β [TGF-β]) and in-stent restenosis, 6 months after femoral PTA with stent implantation. We performed a single-center prospective study with 26 patients with peripheral artery disease requiring PTA and stenting. As control, we studied 26 patients who were submitted to diagnostic angiography. Serum samples were collected before stent implantation, 24 hr and 6 months after the procedure. To detect restenosis, a new angiography was obtained at 6 months. Restenosis was observed in 10 (38.5%) patients who underwent PTA and stenting. There was a trend to increased levels of IL-6, TNF-α, TGF-β, and IL-12 24 hr after PTA and stenting compared with pretreatment. IL-8 levels showed a statistically significant reduction 24 hours after versus pretreatment (P < 0.05), 6 months vs. pretreatment, and 6 months vs. 24 hr (P < 0.01). There was no statistical difference between cytokine levels when comparing restenosis and no restenosis groups. CRP levels were already high at pretreatment. No inflammatory marker was independently identified as risk factor for in-stent restenosis, 6 months after femoral PTA with stent implantation. The question that remains is whether acute phase reactants will be clinically useful to predict the individual risk for in-stent restenosis. Copyright © 2015 Elsevier Inc. All rights reserved.

  8. Identification of Apolipoprotein C-I as a Potential Wilms’ Tumor Marker after Excluding Inflammatory Factors

    PubMed Central

    Zhang, Junjie; Guo, Fei; Wang, Lei; Zhao, Wei; Zhang, Da; Yang, Heying; Yu, Jiekai; Niu, Lili; Yang, Fuquan; Zheng, Shu; Wang, Jiaxiang

    2014-01-01

    Wilms’ tumor is one of the most common malignant tumors observed in children, and its early diagnosis is important for late-stage treatment and prognosis. We previously screened and identified protein markers for Wilms’ tumor; however, these markers lacked specificity, and some were associated with inflammation. In the current study, serum samples from children with Wilms’ tumors were compared with those of healthy controls and patients with systemic inflammatory response syndrome (SIRS). After exclusion of factors associated with inflammation, specific protein markers for Wilms’ tumors were identified. After comparing the protein peak values obtained from all three groups, a protein with a m/z of 6438 Da was specified. Purification and identification of the target protein using high-pressure liquid chromatography (HPLC) and two-dimensional liquid chromatography-linearion trap mass spectrometry(2D-LC-LTQ-MS) mass spectrometry, respectively, revealed that it was apolipoprotein C-I (APO C-I). Thus, APO C-I is a specific protein marker for Wilms’ tumor. PMID:25222555

  9. In situ detection of frequent and active infection of human cytomegalovirus in inflammatory abdominal aortic aneurysms: possible pathogenic role in sustained chronic inflammatory reaction.

    PubMed

    Yonemitsu, Y; Nakagawa, K; Tanaka, S; Mori, R; Sugimachi, K; Sueishi, K

    1996-04-01

    Inflammatory abdominal aortic aneurysm (IAAA) is histopathologically characterized by extensive adventitial fibrosis, mononuclear cell infiltration with lymph follicle formation, and severe atheromatous changes in the aneurysmal wall. We previously reported a frequent prevalence and immediate early gene expression of human cytomegalovirus (CMV) in IAAA by solution-phase PCR and reverse transcription PCR, respectively, and suggested that this virus might play a role in chronic inflammatory reaction in IAAA. To evaluate the pathogenic role of CMV infection, the frequency and distribution of CMV infected cells in IAAA were examined by in situ PCR, and compared with those in atherosclerotic aneurysms (AA) and control cases with minimal atherosclerotic changes. Human leukocyte antigen (HLA)-DR was simultaneously evaluated as a marker for immune response related to CMV infection. Immediate early gene expression was also detected by reverse transcription PCR and in situ hybridization, to certify whether the CMV infection in IAAA is active or latent. In the fibrously thickened adventitia of IAAA, CMV infected cells and HLA-DR-positive cells were more frequently encountered than in that of AA and control cases (p < 0.01). CMV infected cells were largely identified as macrophages, fibroblasts, endothelial cells, and lymphocytes. The expression of CMV immediate early mRNA, which suggests an active infection inducing active inflammatory reaction, was detected in most of the macrophages, endothelial cells, and fibroblasts. Our results strongly suggest that frequent and active infection of CMV in IAAA plays a significant role in the induction and acceleration of chronic inflammatory reaction in aortas of IAAA.

  10. Markers of inflammation, activation of blood platelets and coagulation disorders in inflammatory bowel diseases.

    PubMed

    Matowicka-Karna, Joanna

    2016-04-13

    Inflammatory bowel disease (IBD) includes ulcerative colitis and Crohn's disease. It is a group of chronic disorders characterized by inflammation of the gastrointestinal track with unknown etiology. Currently applied biomarkers include CRP, ESR, pANCA, ASCA, and fecal calprotectin. The etiopathogenesis of IBD is multifactorial. In patients with IBD in inflamed alimentary tract mucosa the number of recruited monocytes and activated macrophages which are source of cytokines. In IBD, the exacerbation is accompanied by thrombocytosis. Platelets play a crucial role in the hemostasis and inflammatory response. Selectins, which regulates the hemostasis and inflammatory response, stimulates the secretion of many inflammatory mediators such as β-thromboglobuline, CD40L, fibrinogen, IL-1β, platelet factor-4. In the course of IBD the following changes are observed: an increase in the number of platelets (reactive thrombocytosis), PDW and PCT, reduction in MPV, increased production and excretion of granular content products (P-selectin, GP53, β-TG, PF-4, vWF, fibrinolytic inhibitors).

  11. Inflammatory and Lipid-Associated Markers of Cardiovascular Diseases in Children with First Exacerbation of Inflammatory Bowel Disease.

    PubMed

    Pac-Kożuchowska, Elżbieta; Krawiec, Paulina; Mroczkowska-Juchkiewicz, Agnieszka; Pawłowska-Kamieniak, Agnieszka; Kominek, Katarzyna

    2016-05-06

    BACKGROUND Adult patients with inflammatory bowel disease (IBD) are at increased risk of early atherosclerosis and atherosclerosis-driven cardiovascular diseases. However, data on the development of early, subclinical atherosclerosis in children with IBD are scarce. The aim of this study was to assess selected biomarkers of atherosclerosis in children with IBD. MATERIAL AND METHODS The study group comprised 30 children with first exacerbation of IBD. Twenty healthy children were enrolled into the control group. Total cholesterol, triglycerides, low-density lipoproteins (LDL), high-density lipoproteins (HDL), lipoprotein (a) (Lp(a)), interleukin 6 (Il-6), high sensitivity C-reactive protein (hs-CRP), and oxidized LDL (ox LDL) were determined. RESULTS There were no significant differences in lipids profiles in IBD children and controls. Mean IL-6 level (8.996 pg/ml) was significantly higher in the IBD group compared to controls (3.502 pg/ml). Mean hs-CRP concentration was significantly higher in IBD children than in controls (7.648 and 1.290 µg/ml, respectively). In the IBD group, mean ox-LDL concentration (144.837 ng/ml) was lower than in controls (162.352 ng/ml), but the difference was non-significant (P=0.4). Mean Lp(a) serum level was higher in patients with IBD (19.418 mg/dl) than in controls (10.970 mg/dl), but it was also non-significant. CONCLUSIONS No significant differences were found in biomarkers of atherosclerosis in children with IBD compared to controls. Elevated IL-6 and hs-CRP level are well-established inflammatory markers. Further studies are needed to fully determine cardiovascular risk factors in IBD children.

  12. Inflammation Markers and Major Depressive Disorder in Patients With Chronic Heart Failure: Results From the Sertraline Against Depression and Heart Disease in Chronic Heart Failure Study.

    PubMed

    Xiong, Glen L; Prybol, Kevin; Boyle, Stephen H; Hall, Russell; Streilein, Robert D; Steffens, David C; Krishnan, Ranga; Rogers, Joseph G; O'Connor, Christopher M; Jiang, Wei

    2015-09-01

    Major depressive disorder (MDD) and chronic heart failure (CHF) have in common heightening states of inflammation, manifested by elevated inflammation markers such as C-reactive protein. This study compared inflammatory biomarker profiles in patients with CHF and MDD to those without MDD. The study recruited patients admitted to inpatient care for acute heart failure exacerbations, after psychiatric diagnostic interview. Patients with Beck Depression Inventory (BDI) scores lower than 10 and with no history of depression served as the nondepressed reference group (n = 25). MDD severity was defined as follows: mild (BDI 10-15; n = 48), moderate (BDI 16-23; n = 51), and severe (BDI ≥ 24; n = 33). A Bio-Plex assay measured 18 inflammation markers. Ordinal logistic models were used to examine the association of MDD severity and biomarker levels. Adjusting for age, sex, statin use, body mass index, left ventricular ejection fraction, tobacco use, and New York Heart Association class, the MDD overall group variable was significantly associated with elevated interleukin (IL)-2 (p = .019), IL-4 (p = .020), IL-6 (p = .026), interferon-γ (p = .010), monocyte chemoattractant protein 1 (p = .002), macrophage inflammatory protein 1β (p = .003), and tumor necrosis factor α (p = .004). MDD severity subgroups had a greater probability of elevated IL-6, IL-8, interferon-γ, monocyte chemoattractant protein 1, macrophage inflammatory protein 1β, and tumor necrosis factor α compared with nondepressed group. The nondepressed group had greater probability of elevated IL-17 (p < .001) and IL-1β (p < .01). MDD in patients with CHF was associated with altered inflammation marker levels compared with patients with CHF who had no depression. Whether effective depression treatment will normalize the altered inflammation marker levels requires further study. ClinicalTrials.gov NCT00078286.

  13. Increased levels of inflammatory plasma markers and obesity risk in a mouse model of Down syndrome.

    PubMed

    Fructuoso, M; Rachdi, L; Philippe, E; Denis, R G; Magnan, C; Le Stunff, H; Janel, N; Dierssen, M

    2017-09-25

    Down syndrome (DS) is caused by the trisomy of human chromosome 21 and is the most common genetic cause of intellectual disability. In addition to the intellectual deficiencies and physical anomalies, DS individuals present a higher prevalence of obesity and subsequent metabolic disorders than healthy adults. There is increasing evidence from both clinical and experimental studies indicating the association of visceral obesity with a pro-inflammatory status and recent studies have reported that obese people with DS suffer from low-grade systemic inflammation. However, the link between adiposity and inflammation has not been explored in DS. Here we used Ts65Dn mice, a validated DS mouse model, for the study of obesity-related inflammatory markers. Ts65Dn mice presented increased energy intake, and a positive energy balance leading to increased adiposity (fat mass per body weight), but did not show overweight, which only was apparent upon high fat diet induced obesity. Trisomic mice also had fasting hyperglycemia and hypoinsulinemia, and normal incretin levels. Those trisomy-associated changes were accompanied by reduced ghrelin plasma levels and slightly but not significantly increased leptin levels. Upon a glucose load, Ts65Dn mice showed normal increase of incretins accompanied by over-responses of leptin and resistin, while maintaining the hyperglycemic and hypoinsulinemic phenotype. These changes in the adipoinsular axis were accompanied by increased plasma levels of inflammatory biomarkers previously correlated with obesity galectin-3 and HSP72, and reduced IL-6. Taken together, these results suggest that increased adiposity, and pro-inflammatory adipokines leading to low-grade inflammation are important players in the propensity to obesity in DS. We conclude that DS would be a case of impaired metabolic-inflammatory axis. Copyright © 2017 Elsevier Inc. All rights reserved.

  14. Surgical treatment of chronic inflammatory bowel disease in children.

    PubMed

    Barrena, S; Martínez, L; Hernandez, F; Lassaletta, L; Lopez-Santamaria, M; Prieto, G; Larrauri, J; Tovar, J A

    2011-04-01

    Surgery for chronic inflammatory bowel disease (IBD) is increasingly often necessary in children. This study aimed at assessing the results of these operations in order to facilitate adequate preoperative counseling. We reviewed patients treated from 1992 to 2009. The operations, complications and functional outcome were recorded. For those with preserved rectal defecation, continence (Koivusalo score) and quality of life (standardized questionnaire) were assessed in the long term. Eighty five of 192 patients had Crohn disease (CD), 107 of 192 had ulcerative colitis (UC), and 3 of 192 had indeterminate colitis (IC). 12 of 85 CD patients (15%) aged 14 (12-19) years required 13 resections, 1 stricturoplasty, 1 transplantation and 6 other operations including 3 permanent enterostomies for anorectal involvement. Removal of the involved bowel led to significant improvement of nutritional status, growth and quality of life. The transplanted patient had a striking recovery but eventually died 1 year later of unrelated complications. 29 of 107 UC patients (26%) aged 11 (2-15) years required 87 operations. Nine had emergency colectomy for toxic megacolon (3, one death) or severe hemorrhage (6). 28 had restorative proctocolectomy and ileoanostomy (RPCIA) without (16) or with (12) J-pouch under protective ileostomy. Complications were frequent (40%). Permanent ileostomy was required in five children (17%). Twelve months postoperatively, RPCIA patients had 6.5 (2-13) stools/day; all were continent during daytime, and 25% have nocturnal leaks. Mean Koivusalo score (5-12) was 8.8 ± 2. Quality of life was good in all. All attended normal school and 7 the university, 4 work and 60% of those older than 18 years have sexual partners. Three of 107 children treated as UC with RPCIA had ultimately IC (3%) and were permanently diverted. The nature of IBD involves frustrating surgery. However, it may change life for CD patients and provide a reasonably good quality of life for UC after

  15. Differential expression of systemic inflammatory mediators in amputees with chronic residual limb pain.

    PubMed

    Chamessian, Alexander; Van de Ven, Thomas; Buchheit, Thomas; Hsia, Hung-Lun; McDuffie, Mary; Gamazon, Eric R; Walsh, Colin; Bruehl, Stephen; Buckenmaier, Chester 'Trip'; Shaw, Andrew

    2017-01-01

    Chronic postsurgical pain impacts most amputees, with more than half experiencing neuralgic residual limb pain. The transition from normal acute postamputation pain to chronic residual limb pain likely involves both peripheral and central inflammatory mechanisms. As part of the Veterans Integrated Pain Evaluation Research study, we investigated links between systemic inflammatory mediator levels and chronic residual limb pain. Subjects included 36 recent active duty military traumatic amputees with chronic residual limb pain and 40 without clinically significant pain. Blood samples were obtained and plasma concentrations of an array of inflammatory mediators were analyzed. Residual limb pain intensity and pain catastrophizing were assessed to examine associations with inflammatory mediators. Pro-inflammatory mediators including tumor necrosis factor (TNF)-α, TNF-β, interleukin (IL)-8, ICAM-1, Tie2, CRP, and SAA were elevated in patients with chronic residual limb pain. Across all patients, residual limb pain intensity was associated positively with levels of several proinflammatory mediators (IL-8, TNF-α, IL-12, TNF-β, PIGF, Tie2, SAA, and ICAM-1), and inversely with concentrations of the anti-inflammatory mediator IL-13, as well as IL-2 and Eotaxin-3. Pain catastrophizing correlated positively with IL-8, IL-12, TNF-β, PIGF, and ICAM-1, and inversely with IL-13. Significant associations between catastrophizing and residual limb pain intensity were partially mediated by TNF-α, TNF- β, SAA, and ICAM-1 levels. Results suggest that chronic postamputation residual limb pain is associated with excessive inflammatory response to injury or to inadequate resolution of the postinjury inflammatory state. Impact of pain catastrophizing on residual limb pain may be because of part to common underlying inflammatory mechanisms.

  16. Serum Clusterin as a Prognostic Marker of Chronic Spontaneous Urticaria.

    PubMed

    Kim, Ji-Hye; Lee, Hyung-Young; Ban, Ga-Young; Shin, Yoo-Seob; Park, Hae-Sim; Ye, Young-Min

    2016-05-01

    A substantial proportion of patients with chronic spontaneous urticaria (CSU) are refractory to antihistamines. However, identifying the subpopulation whose urticaria is not completely controlled by antihistamines remains difficult. The response of autologous serum skin test (ASST), a clinical test for the detection of basophil histamine-releasing activity upon autoantibodies or autoreactive stimulation, has been suggested as a potential predictor in the control of urticaria. We sought to identify proteins that were differentially expressed in the sera of patients with positive and negative ASST results and to investigate their association with urticaria control.Proteomics analysis was performed using sera from 3 CSU patients with positive ASST results compared with those showing negative ASST results. Seven upregulated and 5 downregulated proteins were identified by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry in the ASST-positive group compared with the ASST-negative group.Proteins that were differentially expressed according to the ASST results in CSU patients were classified into 6 groups: apolipoproteins, glycoproteins, modified albumin, haptoglobulin, plectin, and others. Among these, apolipoprotein J or clusterin was validated using an enzyme-linked immunosorbent assay. Clusterin levels in 69 ASST-positive patients were significantly higher than those in 69 ASST-negative patients and in 86 healthy controls (231.2 ± 44.0 vs 210.2 ± 36.1 vs 118.7 ± 71.9 μg/mL, P < 0.001). Furthermore, clusterin levels differed significantly between patients with responsive and refractory responses to antihistamine treatment within 3 months (231.0 ± 39.1 vs 205.1 ± 40.4 μg/mL, P < 0.001). ASST results and serum clusterin levels can predict 92.7% of CSU patients whose urticaria would be refractory to antihistamines. Serum clusterin can be a prognostic marker to determine the responsiveness to antihistamine

  17. Serum Clusterin as a Prognostic Marker of Chronic Spontaneous Urticaria

    PubMed Central

    Kim, Ji-Hye; Lee, Hyung-Young; Ban, Ga-Young; Shin, Yoo-Seob; Park, Hae-Sim; Ye, Young-Min

    2016-01-01

    Abstract A substantial proportion of patients with chronic spontaneous urticaria (CSU) are refractory to antihistamines. However, identifying the subpopulation whose urticaria is not completely controlled by antihistamines remains difficult. The response of autologous serum skin test (ASST), a clinical test for the detection of basophil histamine-releasing activity upon autoantibodies or autoreactive stimulation, has been suggested as a potential predictor in the control of urticaria. We sought to identify proteins that were differentially expressed in the sera of patients with positive and negative ASST results and to investigate their association with urticaria control. Proteomics analysis was performed using sera from 3 CSU patients with positive ASST results compared with those showing negative ASST results. Seven upregulated and 5 downregulated proteins were identified by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry in the ASST-positive group compared with the ASST-negative group. Proteins that were differentially expressed according to the ASST results in CSU patients were classified into 6 groups: apolipoproteins, glycoproteins, modified albumin, haptoglobulin, plectin, and others. Among these, apolipoprotein J or clusterin was validated using an enzyme-linked immunosorbent assay. Clusterin levels in 69 ASST-positive patients were significantly higher than those in 69 ASST-negative patients and in 86 healthy controls (231.2 ± 44.0 vs 210.2 ± 36.1 vs 118.7 ± 71.9 μg/mL, P < 0.001). Furthermore, clusterin levels differed significantly between patients with responsive and refractory responses to antihistamine treatment within 3 months (231.0 ± 39.1 vs 205.1 ± 40.4 μg/mL, P < 0.001). ASST results and serum clusterin levels can predict 92.7% of CSU patients whose urticaria would be refractory to antihistamines. Serum clusterin can be a prognostic marker to determine the responsiveness to

  18. The cervical smear pattern in patients with chronic pelvic inflammatory disease.

    PubMed

    Abdul, M A; Shittu, S O; Randawa, J A; Shehu, M S

    2009-09-01

    Cancer of the cervix is the commonest malignancy of the genital tract in Nigeria. In an atmosphere of opportunistic screening due to lack of a national screening programme, studies are needed to determine patients at risk of premalignant lesions of the cervix. To determine cervical smear pattern in patients with chronic pelvic inflammatory disease and investigate the potential of chronic pelvic inflammatory disease as a risk factor to cervical dysplasia. Case-control study. Department of Obstetrics and Gynaecology, Ahmadu Bello University Teaching Hospital Zaria, Nigeria. Three hundred and sixty-nine premenopausal women attending the gynaecologic and family planning clinics of Ahmadu Bello University Teaching Hospital Zaria, Nigeria from January to December 2000. Of the 369 women that had cervical cytology by Pap smear, 163 (44%) had chronic pelvic inflammatory disease (cases) while 206 (56%) were non chronic PID patients (control). There was no statistical significance in the mean age between the two groups. The mean age at first coitus and marriage of all the women were 17.92.7 years and 18.5 3.4 years respectively. There were 52 dysplastic smears encountered, giving a prevalence rate of 140/1,000 or 14% for Cervical Intraepithelial Neoplasia. There were higher cases of dysplasia in the chronic PID group than in the control and this differences was statistically significant (p<0.05). Other risk factors to dysplasia identified include high parity (>4) and age of first coitus less than 20 years. Only 10% of all the women screened were aware of both cervical cancer and Pap smear. Women with chronic pelvic inflammatory disease are probably at higher risk of developing cervical dysplasia than women without chronic pelvic inflammatory disease. Cervical cancer screening programmes should be intensified in chronic pelvic inflammatory disease patients. However, further studies are needed in our setting to verify the association between pelvic inflammatory disease and

  19. Orthodontic treatment effects on inflammatory marker profiles in saliva before and after 2 archwire changes

    NASA Astrophysics Data System (ADS)

    Yamamoto, Zulham; Jaafar, Ikmal Mohamad; Rohaya, M. A. W.; Abidin, Intan Zarina Zainol; Senafi, Sahidan; Ariffin, Zaidah Zainal; Ariffin, Shahrul Hisham Zainal

    2013-11-01

    Periodontal tissue changes exerted by external forces in orthodontic treatment allow tooth movement. The changes in periodontal tissues i.e. inflammation can be monitored using gingival crevicular fluid (GCF). GCF is a component of saliva. Saliva could be used to monitor periodontal disease progression. The use of saliva to monitor periodontal tissues changes during orthodontic treatment is still unknown. Therefore, we observed the profiles of inflammatory markers namely creatine kinase ('CK), nitric oxide (NO), lactate dehydrogenase (LDH) and aspartate aminotransferase (AST) in saliva of orthodontic patients to evaluate their importance in orthodontic treatment. A total of 21 subjects (13 female and 8 male) participated in this study. Samples were collected from gingival crevicular fluid at three period of archwire changes: baseline (M0), 2 weeks after 0.014" NiTi archwire (M1), and 2 weeks after 0.018" NiTi archwire (M2). All enzyme activities i.e. CK, LDH and AST were measured spectrophotometrically at 340 nm. Griess assay was used to measure nitric oxide level. CK activity, NO level, LDH activity and AST activity in saliva samples did not show significant differences among period of archwire changes. The use of inflammatory marker profiles in saliva may not represent the changes in periodontal tissues during orthodontic treatment.

  20. The hygiene hypothesis and the increasing prevalence of chronic inflammatory disorders.

    PubMed

    Rook, Graham A W

    2007-11-01

    The 'Hygiene' or 'Old Friends' hypothesis suggests that increases in chronic inflammatory disorders (allergies, inflammatory bowel disease and autoimmunity) in developed countries are partly attributable to diminishing exposure to organisms that were part of mammalian evolutionary history. Crucial organisms, including helminths and saprophytic mycobacteria, are recognised by the innate immune system as harmless or, in the case of helminths, as organisms that once established must be tolerated. This recognition then triggers development of regulatory dendritic cells that drive regulatory T-cell responses to the 'Old Friends' themselves and to simultaneously processed 'forbidden' target antigens of the chronic inflammatory disorders.

  1. [Leeching in the treatment of chronic inflammatory and dystrophic diseases of the salivary glands].

    PubMed

    Abal'masov, D V; Afanas'ev, V V; Pozharitskaia, M M

    2003-01-01

    Twenty patients with chronic inflammatory and dystrophic diseases of the salivary glands (sialadenitis, sialadenosis) were examined and treated using hirudotherapy. Positive clinical shifts were observed in 50% patients; the most pronounced therapeutic effect was observed in patients with sialadenosis. Hirudotherapy was ineffective in patients with chronic parenchymatous parotitis paralleled by Sjogren's syndrome.

  2. Intrathecal Dexmedetomidine for Anaesthetic Management of a Patient with Chronic Inflammatory Demyelinating Polyneuropathy

    PubMed Central

    Srinivasalu, D

    2016-01-01

    Chronic demyelinating disorders have multifactorial origin but common important physiologic and anaesthetic considerations. Choice of anaesthesia technique and the drugs used, undertanding the pros and cons of using central neuraxial blocks will help in successful management of such patients. We describe the anaesthetic management of a 34-year-old male with chronic inflammatory demyelinating polyneuropathy posted for cystolithotripsy. PMID:27790558

  3. Source apportionment of particulate matter in the US and associations with lung inflammatory markers

    SciTech Connect

    Duvall, R.M.; Norris, G.A.; Dailey, L.A.; Burke, J.M.; McGee, J.K.; Gilmour, M.I.; Gordon, T.; Devlin, R.B.

    2008-07-01

    Size-fractionated particulate matter (PM) samples were collected from six U.S. cities and chemically analyzed as part of the Multiple Air Pollutant Study. Particles were administered to cultured lung cells and the production of three different proinflammatory markers was measured to explore the association between the health effect markers and PM. Ultrafine, fine, and coarse PM samples were collected between December 2003 and May 2004 over a 4-wk period in each city. Filters were pooled for each city and the PM samples were extracted then analyzed for trace metals, ions, and elemental carbon. Particle extracts were applied to cultured human primary airway epithelial cells, and the secreted levels of interleukin-8 (IL-8), heme oxygenase-1, and cyclooxygenase-2 were measured 1 and 24 h following exposure. Fine PM sources were quantified by the chemical mass balance (CMB) model. The relationship between toxicological measures, PM sources, and individual species were evaluated using linear regression. Ultrafine and fine PM mass were associated with increases in IL-8 (r{sup 2} = .80 for ultrafine and r{sup 2} = .52 for fine). Sources of fine PM and their relative contributions varied across the sampling sites and a strong linear association was observed between IL-8 and secondary sulfate from coal combustion (r{sup 2} = .79). Ultrafine vanadium, lead, copper, and sulfate were also associated with increases in IL-8. Increases in inflammatory markers were not observed for coarse PM mass and source markers. These findings suggest that certain PM size fractions and sources are associated with markers of lung injury or inflammation.

  4. Vitamin E differentially affects short term exercise induced changes in oxidative stress, lipids, and inflammatory markers.

    PubMed

    Garelnabi, M; Veledar, E; White-Welkley, J; Santanam, N; Abramson, J; Weintraub, W; Parthasarathy, S

    2012-10-01

    Physical activity or exercise is a proven deterrent of cardiovascular diseases. The purpose of this study was to examine whether vitamin E supplementation interfere with the potential benefits of exercise. A total of 455 apparently healthy men and women were recruited, for a 2-month aerobic/cardiovascular exercise program. Subjects were randomly assigned for soft gel vitamin E or placebo (800 IU), and required to give blood at 0, 2, 4 and 8 weeks of exercise. Levels of lipid and markers of oxidative stress and inflammation were measured along with the VO2 and duration time spent on treadmill. Statistical analysis did not show significant changes in the levels of lipids and markers of oxidative stress and inflammation. Favorable trends among both of the randomization groups were observed in lipids, and some of the oxidative stress and inflammatory markers. This study also established several interesting correlations between VO2, and lipids on one hand and markers of oxidation and inflammation on the other hand. Reduction in LDL levels positively associated with increased levels of MCP-1 (P < 0.008) among placebo group, and also decreased hCRP levels strongly correlated with the increases in VO2 (P < 0.0004) among the placebo, and vitamin E subjects (P < 0.01). Exercise training induces oxidative stress might be instrumental in favorable lipid reduction and markers of oxidative stress and inflammation. However interestingly, vitamin E didn't demonstrate favorable effects on the level of oxidative stress and inflammation associated with exercise. Copyright © 2011 Elsevier B.V. All rights reserved.

  5. Experimental Gingivitis Induces Systemic Inflammatory Markers in Young Healthy Individuals: A Single-Subject Interventional Study

    PubMed Central

    Luchtefeld, Maren; Heuer, Wieland; Schuett, Harald; Divchev, Dimitar; Scherer, Ralph; Schmitz-Streit, Ruth; Langfeldt, Daniela; Stumpp, Nico; Staufenbiel, Ingmar

    2013-01-01

    Objectives We here investigated whether experimental gingivitis enhances systemic markers of inflammation which are also known as surrogate markers of atherosclerotic plaque development. Background Gingivitis is a low-level oral infection induced by bacterial deposits with a high prevalence within Western populations. A potential link between the more severe oral disease periodontitis and cardiovascular disease has already been shown. Methods 37 non-smoking young volunteers with no inflammatory disease or any cardiovascular risk factors participated in this single-subject interventional study with an intra-individual control. Intentionally experimental oral inflammation was induced by the interruption of oral hygiene for 21 days, followed by a 21-days resolving phase after reinitiation of oral hygiene. Primary outcome measures at baseline, day 21 and 42 were concentrations of hsCRP, IL-6, and MCP-1, as well as adhesion capacity and oxLDL uptake of isolated blood monocytes. Results The partial cessation of oral hygiene procedures was followed by the significant increase of gingival bleeding (34.0%, P<0.0001). This local inflammation was associated with a systemic increase in hsCRP (0.24 mg/L, P = 0.038), IL-6 (12.52 ng/L, P = 0.0002) and MCP-1 (9.10 ng/l, P = 0.124) in peripheral blood samples between baseline and day 21, which decreased at day 42. Monocytes showed an enhanced adherence to endothelial cells and increased foam cell formation after oxLDL uptake (P<0.050) at day 21 of gingivitis. Conclusions Bacterial-induced gingival low-level inflammation induced a systemic increase in inflammatory markers. Dental hygiene almost completely reversed this experimental inflammatory process, suggesting that appropriate dental prophylaxis may also limit systemic markers of inflammation in subjects with natural gingivitis. International Clinical Trials Register Platform of the World Health Organization, registry number: DRKS00003366, URL: http

  6. Challenges and Current Efforts in the Development of Biomarkers for Chronic Inflammatory and Remodeling Conditions of the Lungs

    PubMed Central

    Grunig, Gabriele; Baghdassarian, Aram; Park, Sung-Hyun; Pylawka, Serhiy; Bleck, Bertram; Reibman, Joan; Berman-Rosenzweig, Erika; Durmus, Nedim

    2015-01-01

    This review discusses biomarkers that are being researched for their usefulness to phenotype chronic inflammatory lung diseases that cause remodeling of the lung’s architecture. The review focuses on asthma, chronic obstructive pulmonary disease (COPD), and pulmonary hypertension. Bio-markers of environmental exposure and specific classes of biomarkers (noncoding RNA, metabolism, vitamin, coagulation, and microbiome related) are also discussed. Examples of biomarkers that are in clinical use, biomarkers that are under development, and biomarkers that are still in the research phase are discussed. We chose to present examples of the research in biomarker development by diseases, because asthma, COPD, and pulmonary hypertension are distinct entities, although they clearly share processes of inflammation and remodeling. PMID:26917944

  7. Challenges and Current Efforts in the Development of Biomarkers for Chronic Inflammatory and Remodeling Conditions of the Lungs.

    PubMed

    Grunig, Gabriele; Baghdassarian, Aram; Park, Sung-Hyun; Pylawka, Serhiy; Bleck, Bertram; Reibman, Joan; Berman-Rosenzweig, Erika; Durmus, Nedim

    2015-01-01

    This review discusses biomarkers that are being researched for their usefulness to phenotype chronic inflammatory lung diseases that cause remodeling of the lung's architecture. The review focuses on asthma, chronic obstructive pulmonary disease (COPD), and pulmonary hypertension. Bio-markers of environmental exposure and specific classes of biomarkers (noncoding RNA, metabolism, vitamin, coagulation, and microbiome related) are also discussed. Examples of biomarkers that are in clinical use, biomarkers that are under development, and biomarkers that are still in the research phase are discussed. We chose to present examples of the research in biomarker development by diseases, because asthma, COPD, and pulmonary hypertension are distinct entities, although they clearly share processes of inflammation and remodeling.

  8. Inflammatory markers and risk of epithelial ovarian cancer by tumor subtypes: the EPIC cohort

    PubMed Central

    Ose, Jennifer; Schock, Helena; Tjonneland, Anne; Hansen, Louise; Overvad, Kim; Dossus, Laure; Clavel-Chapelon, Francoise; Baglietto, Laura; Boeing, Heiner; Trichopolou, Antonia; Benetou, Vassiliki; Lagiou, Pagona; Masala, Giovanna; Tagliabue, Giovanna; Tumino, Rosario; Sacerdote, Carlotta; Mattiello, Amalia; de Mesquita, H.Bas Bueno; Peeters, Petra H M; Onland-Moret, N Charlotte; Weiderpass, Elisabete; Gram, Inger T; Sánchez, Soledad; Obon-Santacana, Mireia; Sànchez-Pérez, Maria-José; Larrañaga, Nerea; Castaño, José María Huerta; Ardanaz, Eva; Brändstedt, Jenny; Lundin, Eva; Idahl, Annika; Travis, Ruth C; Khaw, Kay-Tee; Rinaldi, Sabina; Romieu, Isabelle; Merrit, Melissa A; Gunter, Marc J; Riboli, Elio; Kaaks, Rudolf; Fortner, Renée T

    2015-01-01

    Background Evidence suggests an etiologic role for inflammation in ovarian carcinogenesis and heterogeneity between tumor subtypes and anthropometric indices. Prospective studies on circulating inflammatory markers and epithelial invasive ovarian cancer (EOC) have predominantly investigated overall risk; data characterizing risk by tumor characteristics (histology, grade, stage, dualistic model of ovarian carcinogenesis) and anthropometric indices are sparse. Methods We conducted a nested case-control study in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort to evaluate C-reactive protein (CRP), interleukin-6 (IL-6), and EOC risk by tumor characteristics. A total of 754 eligible EOC cases were identified; two controls (n=1,497) were matched per case. We used multivariable conditional logistic regression to assess associations. Results CRP and IL-6 were not associated with overall EOC risk. However, consistent with prior research, CRP >10 vs. CRP ≤1 mg/L was associated with higher overall EOC risk (OR=1.67 [1.03 - 2.70]). We did not observe significant associations or heterogeneity in analyses by tumor characteristics. In analyses stratified by waist circumference, inflammatory markers were associated with higher risk among women with higher waist circumference; no association was observed for women with normal waist circumference: (e.g., IL-6: waist ≤80: ORlog2=0.97 [0.81 - 1.16]; waist >88: ORlog2=1.78 [1.28 - 2.48], pheterogeneity ≤0.01). Conclusions Our data suggest that high CRP is associated with increased risk of overall EOC, and that IL-6 and CRP may be associated with EOC risk among women with higher adiposity. Impact Our data add to global evidence that ovarian carcinogenesis may be promoted by an inflammatory milieu. PMID:25855626

  9. Inflammatory markers and haptoglobin polymorphism in Saudi with non-insulin-dependent diabetes mellitus.

    PubMed

    Mohieldein, Abdelmarouf; Alzohairy, Mohammad; Hasan, Marghoob; Khan, Amjad A

    2012-11-11

    Haptoglobin (Hp) polymorphism associated with clinical evolution of several inflammatory diseases and considered as a predictive factor for development of diabetes complications. We designed the present study to investigate the frequency distribution of Hp phenotypes among Saudi with non-insulin-dependent diabetes mellitus compared to healthy nondiabetic subjects. Moreover, we explored the possibility of relationship between serum levels of inflammatory markers (namely, high-sensitive C-reactive proteins "hs-CRP", interleukin (IL)-6, and Hp) and Hp phenotypes. In the present case-control study, we enrolled 60 type 2 diabetic patients as the study group and 60 healthy subjects as the control group. We assayed serum levels of Hp and hs-CRP by immunoturbidimetric method; while IL-6 was measured by ELISA. Native polyacrylamide gel electrophoresis was used for determination of Hp phenotypes. In type 2 diabetics, serum concentrations of IL-6, hs-CRP, and Hp were significantly elevated and correlated to body mass index. Moreover, there was a significant correlation between plasma glucose level and Hp (r = 0.577, p = 0.000), IL-6 (r = 0.448, p = 0.000), and hs-CRP (r = 0.380, p = 0.001). In addition, data demonstrated a positive correlation between HbA1c and Hp (r = 0.521, p = 0.000), IL-6 (r = 0.420, p = 0.001), and hs-CRP (r = 0.353, p = 0.008). Hp 2-1 phenotype predominated among subjects in both study and control groups. No significant association between Hp phenotypes with any of the investigated inflammatory markers was documented. Inflammation may represent the link between type 2 diabetes and obesity. Hp 2-1 was the predominant phenotype among Saudi type 2 diabetics as well as healthy subjects. In addition to Hp; other possible genetic polymorphisms like CRP may have its effect on diabetes through different mechanisms.

  10. Effect of pulsed electromagnetic field on inflammatory pathway markers in RAW 264.7 murine macrophages.

    PubMed

    Ross, Christina L; Harrison, Benjamin S

    2013-01-01

    In the treatment of bacterial infections, antibiotics have proven to be very effective, but the way in which antibiotics are dosed can create a lag time between the administration of the drug and its absorption at the site of insult. The time it takes an antibiotic to reach therapeutic levels can often be significantly increased if the vascular system is compromized. Bacteria can multiply pending the delivery of the drug, therefore, developing treatments that can inhibit the inflammatory response while waiting for antibiotics to take effect could help prevent medical conditions such as septic shock. The aim of this study was to examine the effect of a pulsed electromagnetic field on the production of inflammatory markers tumor necrosis factor (TNF), transcription factor nuclear factor kappa B (NFkB), and the expression of the A20 (tumor necrosis factor-alpha-induced protein 3), in an inflamed-cell model. Lipopolysaccharide-challenged cells were exposed to a pulsed electromagnetic field at various frequencies in order to determine which, if any, frequency would affect the TNF-NFkB-A20 inflammatory response pathway. Our study revealed that cells continuously exposed to a pulsed electromagnetic field at 5 Hz demonstrated significant changes in the downregulation of TNF-α and NFkB and also showed a trend in the down regulation of A20, as compared with controls. This treatment could be beneficial in modulating the immune response, in the presence of infection.

  11. Effect of pulsed electromagnetic field on inflammatory pathway markers in RAW 264.7 murine macrophages

    PubMed Central

    Ross, Christina L; Harrison, Benjamin S

    2013-01-01

    In the treatment of bacterial infections, antibiotics have proven to be very effective, but the way in which antibiotics are dosed can create a lag time between the administration of the drug and its absorption at the site of insult. The time it takes an antibiotic to reach therapeutic levels can often be significantly increased if the vascular system is compromized. Bacteria can multiply pending the delivery of the drug, therefore, developing treatments that can inhibit the inflammatory response while waiting for antibiotics to take effect could help prevent medical conditions such as septic shock. The aim of this study was to examine the effect of a pulsed electromagnetic field on the production of inflammatory markers tumor necrosis factor (TNF), transcription factor nuclear factor kappa B (NFkB), and the expression of the A20 (tumor necrosis factor-alpha-induced protein 3), in an inflamed-cell model. Lipopolysaccharide-challenged cells were exposed to a pulsed electromagnetic field at various frequencies in order to determine which, if any, frequency would affect the TNF-NFkB-A20 inflammatory response pathway. Our study revealed that cells continuously exposed to a pulsed electromagnetic field at 5 Hz demonstrated significant changes in the downregulation of TNF-α and NFkB and also showed a trend in the down regulation of A20, as compared with controls. This treatment could be beneficial in modulating the immune response, in the presence of infection. PMID:23576877

  12. Serum levels of soluble urokinase plasminogen activator receptor as a new inflammatory marker in adolescent obesity.

    PubMed

    Can, Ummugulsum; Buyukinan, Muammer; Yerlikaya, Fatma Humeyra

    2017-03-01

    Obesity is known for low-grade inflammatory state with enhanced production of inflammatory mediators in children and adolescents. Soluble urokinase plasminogen activator receptor (suPAR) can be generated as a pro-inflammatory marker. This study was conducted to evaluate the role of suPAR, and its association with leptin, adiponectin, interleukin-6 (IL-6), high-sensitive C-reactive protein (hsCRP) and fibrinogen in adolescent obesity. A total of 98 participants, 55 obese individuals and 43 healthy controls, aged between 10 and 17 yr, were included in the study. Serum suPAR, IL-6, leptin and adiponectin were measured using ELISA method. Serum suPAR, IL-6, fibrinogen, hsCRP and leptin levels in obese individuals were significantly higher than those of controls (P<0.05 & P<0.001). Serum adiponectin levels in obese individuals were significantly lower than those of controls (P<0.01). Our findings showed that suPAR, IL-6, fibrinogen, hsCRP and leptin were significantly higher in the obese individuals than those of controls. suPAR may be a good novel biomarker for systemic subclinical inflammation and immune activation linked to adolescent obesity.

  13. Non-surgical periodontal therapy lowers serum inflammatory markers: a pilot study.

    PubMed

    Hussain Bokhari, Syed Akhtar; Khan, Ayyaz Ali; Tatakis, Dimitris N; Azhar, Mohammad; Hanif, Mohammad; Izhar, Mateen

    2009-10-01

    Evidence suggests an association between periodontal disease and coronary heart disease (CHD). C-reactive protein (CRP), fibrinogen, and white blood cell (WBC) counts are markers of inflammation, and their systemic levels have been associated with CHD risk. This pilot study investigated the effect of non-surgical periodontal therapy on systemic levels of CRP, fibrinogen, and WBC counts in subjects with CHD or no CHD (NCHD). Twenty-seven angiographically defined patients with CHD and 18 subjects with NCHD aged >or=40 years were recruited for the study. Periodontal disease was measured through the clinical parameters bleeding on probing (BOP) and probing depth (PD). All subjects received non-surgical periodontal therapy that included oral hygiene instructions and subgingival scaling and root planing. Systemic levels of inflammatory markers (CRP, fibrinogen, and WBC counts) were measured prior to and 1 month after periodontal therapy. Seventeen subjects with CHD and 11 subjects with NCHD completed the study. Subjects with CHD or NCHD experienced significant reductions in BOP (59% and 34%, respectively; P <0.05) and PD (41% and 35%, respectively; P <0.05), with non-significant intergroup differences (P >0.05). In all subjects, CRP, fibrinogen, and WBC counts were reduced significantly (21% to 40%) after periodontal therapy (P <0.05). Periodontal treatment resulted in significant decreases in BOP and PD and lowered serum inflammatory markers in patients with CHD or NCHD. This may result in a decreased risk for CHD in the treated patients. These findings will allow pursuit of a large-scale randomized intervention trial in this population.

  14. Obesity as a Risk and Severity Factor in Rheumatic Diseases (Autoimmune Chronic Inflammatory Diseases)

    PubMed Central

    Gremese, Elisa; Tolusso, Barbara; Gigante, Maria Rita; Ferraccioli, Gianfranco

    2014-01-01

    The growing body of evidence recognizing the adipose tissue (AT) as an active endocrine organ secreting bioactive mediators involved in metabolic and inflammatory disorders, together with the global epidemic of overweight and obesity, rise obesity as a hot topic of current research. The chronic state of low-grade inflammation present in the obese condition and the multiple pleiotropic effects of adipokines on the immune system has been implicated in the pathogenesis of several inflammatory conditions including rheumatic autoimmune and inflammatory diseases. We will discuss the main relevant evidences on the role of the AT on immune and inflammatory networks and the more recent evidences regarding the effects of obesity on the incidence and outcomes of the major autoimmune chronic inflammatory diseases. PMID:25426122

  15. Different pro-inflammatory and immunogenic potentials of Propionibacterium acnes and Staphylococcus epidermidis: implications for chronic inflammatory acne.

    PubMed

    Białecka, Anna; Mak, Monika; Biedroń, Rafał; Bobek, Małgorzata; Kasprowicz, Andrzej; Marcinkiewicz, Janusz

    2005-01-01

    Propionibacterium acnes (PA) and Staphyloccocus epidermidis (SE) are two major bacterial strains isolated from acne lesions. Nevertheless, only PA seems to be implicated in the pathogenesis of inflammatory acne vulgaris. Evidence for this, however, remains indirect and the precise role of PA in inflammatory acne is still a matter for conjecture. The aim of this study was to compare some pro-inflammatory and adjuvant properties of PA and SE. To determine some of the pathogenic, immunostimulatory, and pro-inflammatory proper of PA and SE, two experimental models of inflammation were used. In vivo; chronic inflammation was induced by intradermal injection of living bacteria into the ear. In vitro; peritoneal macrophages elicited by the bacteria were examined for their ability to generate reactive oxygen species (ROS), nitric oxide (NO), and cytokines. PA, but not SE, evoked mild local inflammation of infected ears. Macrophages elicited with PA produced more tumor necrosis factor alpha and interleukin IL-12 than those induced with SE, while SE was a stronger inducer of IL-10 production. Both bacteria equally induced the generation of NO and ROS. In contrast, only PA showed adjuvant proper-ties. The results of these studies indicate that SE, in contrast to PA, does not exert pro-inflammatory properties. Thus it is unlikely that SE may be implicated in the pathogenesis of inflammatory acne vulgaris.

  16. Genetic Markers Associated with Clinical Outcomes in Patients with Inflammatory Bowel Disease.

    PubMed

    Yamamoto-Furusho, Jesús K; Fonseca-Camarillo, Gabriela

    2015-11-01

    Genetic factors play a significant role in determining inflammatory bowel disease (IBD) susceptibility. Epidemiologic data support genetic contribution to the pathogenesis of IBD, which include familial aggregation, twin studies, and racial and ethnic differences in disease prevalence. Recently, several new genes have been identified to be involved in the genetic susceptibility to IBD. The characterization of novel genes potentially will lead to the identification of therapeutic agents and clinical assessment of phenotype and prognosis in patients with IBD. The development of genetic markers associated with clinical outcomes in patients with IBD will be very important in the future. The progress of molecular biology tools (microarrays, proteomics, and epigenetics) have progressed the field of the genetic markers discovery. The advances in bioinformatics coupled with cross-disciplinary collaborations have greatly enhanced our ability to retrieve, characterize, and analyze large amounts of data generated by the technological advances. The techniques available for markers development are genomics (single nucleotide polymorphism genotyping, pharmacogenetics, and gene expression analyses) and proteomics. This could be a potential great benefit in predicting the course of disease in individual patients and in guiding appropriate medical therapy.

  17. Utility of serological markers in inflammatory bowel diseases: gadget or magic?

    PubMed

    Papp, Maria; Norman, Gary L; Altorjay, Istvan; Lakatos, Peter Laszlo

    2007-04-14

    The panel of serologic markers for inflammatory bowel diseases (IBD) is rapidly expanding. Although anti-Saccharomyces cerevisiae antibodies (ASCA) and atypical perinuclear antineutrophil cytoplasmic antibodies (P-ANCA) remain the most widely investigated, an increasing amount of experimental data is available on newly discovered antibodies directed against various microbial antigens. The role of the assessment of various antibodies in the current IBD diagnostic algorithm is often questionable due to their limited sensitivity. In contrast, the association of serologic markers with disease behavior and phenotype is becoming increasingly well-established. An increasing number of observations confirms that patients with Crohn's disease expressing multiple serologic markers at high titers are more likely to have complicated small bowel disease (e.g. stricture and/or perforation) and are at higher risk for surgery than those without, or with low titers of antibodies. Creating homogenous disease sub-groups based on serologic response may help develop more standardized therapeutic approaches and may help in a better understanding of the pathomechanism of IBD. Further prospective clinical studies are needed to establish the clinical role of serologic tests in IBD.

  18. The Relationship between Inflammatory Marker Levels and Hepatitis C Virus Severity

    PubMed Central

    He, Qitian; He, Quan; Qin, Xue; Li, Shan; Li, Taijie; Xie, Li; Deng, Yan; He, Yu

    2016-01-01

    Background. Red cell distribution width (RDW) and platelet-lymphocyte ratio (PLR) have been studied in a variety of etiological diseases. We aim to investigate the relationship between RDW and PLR and the severity of hepatitis C virus- (HCV-) related liver disease. Methods. We included fifty-two chronic HCV and 42 HCV-related cirrhosis patients and 84 healthy controls. Hematological and virological parameters and liver function biomarkers of HCV-related patients at admission were recorded. Results. RDW, RDW-to-platelet (RPR), and 1/PLR values in HCV-related cirrhosis patients were significantly higher than in chronic HCV patients and healthy controls (all P < 0.001). The aspartate aminotransferase (AST)/alanine aminotransferase (ALT) ratio (AAR), AST-to-platelet ratio index (APRI), and fibrosis index based on the four factors (FIB-4) scores in HCV-related cirrhosis patients were significantly higher than in chronic HCV patients (all P < 0.001). The areas under the curve of the RDW, RPR, and 1/PLR for predicting cirrhosis were 0.791, 0.960, and 0.713, respectively. Bivariate logistic regression analysis showed that RDW could independently predict the presence of cirrhosis in chronic HCV patients. Conclusions. RDW, RPR, and PLR may be potential markers for estimating HCV severity. PMID:28090206

  19. The anti-inflammatory effect of locally delivered nano-doxycycline gel in therapy of chronic periodontitis.

    PubMed

    Madi, Marwa; Pavlic, Verica; Samy, Wael; Alagl, Adel

    2017-09-29

    To date, various drugs as host modulating agents had been suggested as adjunctive treatment modality in the therapy of chronic periodontal disease. In this study, the anti-inflammatory effect of subgingivally delivered nanostructured doxycycline gel (nDOX) was evaluated and compared to conventional doxycycline gel (DOX) used as adjunct to scaling and root planning (SRP) in the treatment of moderate chronic periodontitis to reduce probing pocket depth. Nanostructured doxycycline gel (nDOX) was prepared using spray-drying technique with chitosan (CH) as a matrix polymer, followed by dispersion in polyvinyl alcohol (PVA). The deepest periodontal pocket in 45 patients suffering from moderate chronic periodontitis was selected. The patients were divided into three groups following scaling and root planning (SRP); group I: SRP + nDOX, group II: SRP + DOX and group III: SRP + placeboCH. Plaque Index (PI), Gingival Index (GI), pocket depth (PD) and clinical attachment level(CAL), as well as ginigival crevicular fluid levels of (GCF) IL-6 and TNF-α were assessed at baseline, 1 and 3 months following local drug application. Group I showed significant reduction in probing depth and attachment gain compared with group II and III at one and three months period. The inflammatory mediators levels were significantly reduced in all treatment groups at one-month period. Except for group I, the reduced values were observed at three-month period. The results suggest that treatment with nDOX gel as an adjunct to SRP had anti-inflammatory effect by improving both clinical parameters and inflammatory markers up to three months period.

  20. Quercetin prevents chronic unpredictable stress induced behavioral dysfunction in mice by alleviating hippocampal oxidative and inflammatory stress.

    PubMed

    Mehta, Vineet; Parashar, Arun; Udayabanu, Malairaman

    2017-03-15

    It is now evident that chronic stress is associated with anxiety, depression and cognitive dysfunction and very few studies have focused on identifying possible methods to prevent these stress-induced disorders. Previously, we identified abundance of quercetin in Urtica dioica extract, which efficiently attenuated stress related complications. Therefore, current study was designed to investigate the effect of quercetin on chronic unpredicted stress (CUS) induced behavioral dysfunction, oxidative stress and neuroinflammation in the mouse hippocampus. Animals were subjected to unpredicted stress for 21days, during which 30mg/kg quercetin was orally administered to them. Effect of CUS and quercetin treatment on animal behavior was assessed between day 22-26. Afterward, the hippocampus was processed to evaluate neuronal damage, oxidative and inflammatory stress. Results revealed that stressed animals were highly anxious (Elevated Plus Maze and Open Field), showed depressive-like behavior (sucrose preference task), performed poorly in short-term and long-term associative memory task (passive avoidance step-through task) and displayed reduced locomotion (open field). Quercetin alleviated behavioral dysfunction in chronically stressed animals. Compared to CUS, quercetin treatment significantly reduced anxiety, attenuated depression, improved cognitive dysfunction and normalized locomotor activity. Further, CUS elevated the levels of oxidative stress markers (TBARS, nitric oxide), lowered antioxidants (total thiol, catalase), enhanced expression of pro-inflammatory cytokines (IL-6, TNF-α, IL-1β and COX-2) in the hippocampus and damaged hippocampal neurons. Quercetin treatment significantly lowered oxidative and inflammatory stress and prevented neural damage. In conclusion, quercetin can efficiently prevent stress induced neurological complications by rescuing brain from oxidative and inflammatory stress. Copyright © 2017 Elsevier Inc. All rights reserved.

  1. PLASMA LEVELS OF INFLAMMATORY MARKERS NEOPTERIN, SIALIC ACID AND C-REACTIVE PROTEIN IN PREGNANCY AND PREECLAMPSIA

    PubMed Central

    von Versen-Hoeynck, Frauke M.; Hubel, Carl A.; Gallaher, Marcia J.; Gammill, Hilary S.; Powers, Robert W.

    2009-01-01

    Objective To determine whether the cellular inflammatory marker of activated macrophages and monocytes, neopterin (NEO) and the acute phase inflammatory markers sialic acid (SA) and C-reactive protein (CRP) are elevated in pregnancy and further elevated in the pregnancy syndrome preeclampsia. Methods Maternal plasma concentrations of NEO, SA and CRP were measured by high sensitivity ELISA or HPLC in 20 non-pregnant women, 40 women with uncomplicated pregnancies, 50 women with transient hypertension of pregnancy alone, 49 women with small for gestational age (SGA) infants without preeclampsia, and 47 women with preeclampsia. Results The mean concentration of plasma NEO, SA and CRP were all significantly elevated in all groups of pregnant women compared to non-pregnant women (p<0.001 for all). In addition, maternal plasma NEO concentrations were further elevated in women with preeclampsia compared to the other groups of pregnant women (p<0.01). As expected, the acute phase inflammatory markers CRP and SA correlated positively with each other. However, CRP was also correlated with the activated macrophage and monocyte marker NEO in women with transient hypertension of pregnancy and women with preeclampsia (p<0.05). Conclusion The inflammatory markers NEO, SA and CRP are all elevated during pregnancy. However, only NEO, a marker of macrophage and monocyte activation, was further elevated in women with preeclampsia. These data suggest that there is a striking increase in inflammation during pregnancy, and cellular immune activation is further elevated during preeclampsia. PMID:19282816

  2. Does Everything That's Counted Count? Value of Inflammatory Markers for Following Therapy and Predicting Outcome in Diabetic Foot Infection.

    PubMed

    Ong, Eric; Farran, Sumaya; Salloum, Michelle; Gardner, Summer; Giovinco, Nicholas; Armstrong, David G; Matthias, Kathryn R; Nix, David E; Al Mohajer, Mayar

    2017-06-01

    To assess the severity of inflammation associated with diabetic foot infection (DFI), values of inflammatory markers such as white blood count (WBC), C-reactive protein (CRP), erythrocyte sedimentation rate (ESR), and neutrophil to lymphocyte ratio (NLR) are often measured and tracked over time. It remains unclear if these markers can aid the clinician in the diagnosis and management of DFI, and ensure more rational use of antibiotics. Hospitalized adult patients (n = 379) with DFI were retrospectively assessed for abnormal inflammatory markers, correlation between values of inflammatory markers, and clinical diagnosis on initial admission and on last follow-up. At admission, WBC, ESR and NLR were each elevated in patients with osteomyelitis and only ESR was significantly elevated in patients with soft tissue infection only. Only WBC was significantly elevated in patients with osteomyelitis compared with uninfected diabetic feet on last follow-up. Considering the predictive performance of these inflammatory markers, they demonstrated excellent positive predictive value at admission, and excellent negative predictive value at the last follow-up visit. Moreover, the number of elevated markers was further associated with probability of infection both at admission and last follow-up.

  3. Treatment of chronic immune-mediated neuropathies: chronic inflammatory demyelinating polyradiculoneuropathy, multifocal motor neuropathy, and the Lewis-Sumner syndrome.

    PubMed

    Sederholm, Benson H

    2010-09-01

    Current treatment approaches for the management of chronic immune-mediated peripheral neuropathies are reviewed, including chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), multifocal motor neuropathy (MMN), and the Lewis-Sumner syndrome (LSS). A summary of existing evidence for commonly used treatment modalities, such as corticosteroids, intravenous immune globulin (IVIG), and plasma exchange is provided. Evidence for the use of additional immunosuppressant and immunomodulatory agents is also reviewed.

  4. Potential anti-inflammatory effects of maraviroc in HIV-positive patients: a pilot study of inflammation, endothelial dysfunction, and coagulation markers.

    PubMed

    Francisci, Daniela; Falcinelli, Emanuela; Baroncelli, Silvia; Petito, Eleonora; Cecchini, Enisia; Weimer, Liliana Elena; Floridia, Marco; Gresele, Paolo; Baldelli, Franco

    2014-06-01

    Persistent immune activation and chronic inflammation significantly contribute to non-AIDS morbidity in HIV-infected patients. The HIV inhibitor maraviroc (MVC) targets the cellular chemokine CCR5 HIV co-receptor, which is involved in important inflammatory pathways. MVC could have significant anti-inflammatory and anti-atherosclerotic effects, also reducing immune activation. We designed a pilot study to determine which plasma biomarkers of inflammation, endothelial dysfunction, and hypercoagulability were modified by MVC in 2 groups of 10 patients starting MVC-free or MVC-containing regimens. Ten age- and gender-matched healthy controls were also included. We found higher levels of all inflammatory biomarkers in HIV-infected patients compared to healthy controls. Both groups showed decreasing levels of interleukin (IL)-17, IL-10, and macrophage inflammatory protein (MIP)-1a following the achievement of viral suppression. Vascular cell adhesion molecule (VCAM)-1 levels were decreased in the MVC group and increased in the MVC-free group. In conclusion, some inflammatory biomarkers tend to decrease with the salvage regimen; MVC was not associated with a better impact on these measured markers.

  5. The actin-bundling protein L-plastin: a novel local inflammatory marker associated with periodontitis.

    PubMed

    Öztürk, V Ö; Emingil, G; Osterwalder, V; Bostanci, N

    2015-06-01

    L-plastin, an actin-bundling protein, is exclusively expressed in leukocytes and plays a crucial role in immune-mediated events. Periodontitis is a common infectious inflammatory disease that destroys the tooth-supporting tissues. Recent findings using proteomic technologies have demonstrated that L-plastin is one of the few molecules consistently present in the inflammatory exudate of the gingiva in periodontal disease, but not in health. Therefore, this study aimed to investigate in detail the local and systemic role of this molecule in different forms of periodontitis. A total of 61 subjects who met the inclusion/exclusion criteria were recruited, including 21 with chronic periodontitis, 20 generalized aggressive periodontitis and 20 nonperiodontitis control subjects. Gingival tissue biopsies, gingival crevicular fluid, as well as serum and saliva, were obtained. Immunohistochemistry and quantitative real-time PCR were employed to evaluate the localization and mRNA expression, respectively, of L-plastin. L-plastin levels in gingival crevicular fluid, saliva and serum were measured using ELISA. Statistical analysis was performed using nonparametric methods. Subjects with chronic periodontitis and generalized aggressive periodontitis exhibited significantly higher tissue L-plastin gene expression and gingival crevicular fluid levels than did subjects in the control group but there was no significant difference between the two forms of periodontitis. Within gingival tissue, L-plastin was confined to the inflammatory infiltrate. There was no statistically significant difference between serum and salivary L-plastin levels among the three study groups. The elevated gingival tissue expression and gingival crevicular fluid levels of L-plastin in both forms of periodontitis may denote the localized involvement of this novel molecule in the pathogenesis of the disease. © 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

  6. Inflammatory markers are associated with inhibitory avoidance memory deficit induced by sleep deprivation in rats.

    PubMed

    Esumi, L A; Palma, B D; Gomes, V L; Tufik, S; Hipólide, D C

    2011-08-01

    Sleep deprivation (SD) causes detrimental effects to the body, such as memory impairment and weight loss. SD also changes the concentration of inflammatory mediators such as cytokines, which, in turn, can affect cognitive functioning. Thus, the objective of this study was to investigate the involvement of these inflammatory mediators in inhibitory avoidance memory deficit in sleep-deprived rats. Male Wistar rats were deprived of sleep by the modified multiple platform method for 96 h, while their respective controls remained in their housing cages. To assess memory after SD, all animals underwent training, followed by the inhibitory avoidance task test 24h later. Also, the weight of each animal was recorded daily. In the first experiment, animals received an acute administration of lipopolysaccharide (LPS, 50 or 75 μg/kg i.p.) 3h before the inhibitory avoidance training. In the experiment 2, the animals received acute or chronic administration of anti-IL-6 antibody (Ab, 2 μg/kg i.p.). The acute administration was performed 3h before the inhibitory avoidance training, while the chronic treatment administrations were performed daily during the SD period. The 75 μg/kg dose of LPS, but not the 50 μg/kg dose, caused a significant attenuation of memory impairment in the sleep-deprived animals. Although the treatments with the anti-IL-6 Ab did not produce any significant changes in cognitive performance, the Ab attenuated weight loss in sleep-deprived animals. Taken together, these results suggest the involvement of inflammatory mediators in the modulation of memory deficit and weight loss that are observed in sleep-deprived rats. Copyright © 2011 Elsevier B.V. All rights reserved.

  7. Intakes and sources of dietary sugars and their association with metabolic and inflammatory markers.

    PubMed

    O'Connor, Laura; Imamura, Fumiaki; Brage, Soren; Griffin, Simon J; Wareham, Nicholas J; Forouhi, Nita G

    2017-06-17

    Associations of dietary sugars with metabolic and inflammatory markers may vary according to the source of the sugars. The aim of this study was to examine the association of dietary sugars from different sources [beverages (liquids), foods (solids), extrinsic (free) or intrinsic (non-free)] with metabolic and inflammatory markers. Population-based cross-sectional study of adults in the East of England (n = 9678). Sugar intakes were estimated using food frequency questionnaires. Fasting glycated haemoglobin, glucose, insulin, and C-Reactive Protein (CRP) were measured and indices of metabolic risk were derived (homeostatic model of insulin resistance, HOMA-IR and metabolic risk z-score). In multiple linear regression analyses adjusted for potential confounders including BMI and TEI, sugars from liquids were positively associated with ln-CRP [b-coefficient (95%CI), 0.14 (0.05,0.22) per 10%TEI] and metabolic risk z-score [0.13 (0.07,0.18)]. Free sugars were positively associated with ln-HOMA-IR [0.05 (0.03,0.08)] and metabolic risk z-score [0.09 (0.06,0.12)]. Sugars from solids were not associated with any outcome. Among major dietary contributors to intakes (g/d), sugars in fruit, vegetables, dairy products/egg dishes, cakes/biscuits/confectionary and squash/juice drinks were not associated, but sugar added to tea, coffee, cereal was significantly positively associated with all outcomes. Sugars in 100% juice [0.16 (0.06,0.25) per 10%TEI] and other non-alcoholic beverages [0.13 (0.03,0.23)] were positively associated with metabolic risk z-score. Higher intakes of sugars from non-alcoholic beverages and sugar added to tea, coffee, cereal were associated with glycaemia and inflammatory markers. Sugars from solids were not associated, irrespective of whether they were intrinsic or extrinsic. Positive associations of free sugars were largely explained by contribution of beverages to intake. Copyright © 2017 The Author(s). Published by Elsevier Ltd.. All rights

  8. Effects of prandial challenge on triglyceridemia, glycemia, and pro-inflammatory activity in persons with chronic paraplegia

    PubMed Central

    Ellenbroek, Dennis; Kressler, Jochen; Cowan, Rachel E.; Burns, Patricia A.; Mendez, Armando J.; Nash, Mark S.

    2015-01-01

    Context/Objective Exaggerated postprandial lipemia has been reported after spinal cord injury (SCI). We examined metabolite and accompanying pro-inflammatory biomarker responses to repeat feeding of typical high-fat meals in individuals with chronic paraplegia. Design Descriptive trial. Methods Metabolites (triglycerides, glucose, and insulin) and inflammatory biomarkers (interleukin-6 and high-sensitivity C-reactive protein (hsCRP)) were measured under fasting conditions in 11 recreationally active individuals with chronic (>1 year) paraplegia. Subjects received high-fat meals at time point 0 and again at minute 240. Antecubital venous blood was obtained at time points −30 (fasting), 0 (first meal), 30, 60, 90, 120, 240 (second meal), 360, and 480 minutes. Correlations were examined among the study variables. Exploratory subgroup analysis was performed for subjects with levels of postprandial glucose greater than >200 mg/dl. Results Triglycerides showed a significant rise 4 hours after eating. Basal inflammatory markers were elevated, and did not undergo additional change during the testing. Additionally, subjects with excessive postprandial glucose responses showed higher hsCRP levels than those having typical glucose responses both for fasting (11.8 ± 6.5 vs. 2.9 ± 2.7 mg/l, P = 0.064) and postprandial (11.1 ± 4.9 vs. 3.7 ± 3.8 mg/l, P = 0.018) values. Conclusions Despite elevations in metabolic response markers, inflammatory markers did not change significantly after consumption of population-representative (i.e. hypercaloric) mixed-nutrient meals. Levels of fasting CRP in the high-risk range are consistent with other reports in persons with SCI and continue to pose concern for their cardiovascular disease risk. The possible association between postprandial metabolic responses and inflammatory states warrants further investigation to identify individual component risks for this secondary health hazard. PMID:24617559

  9. Diabetic foot syndrome: Immune-inflammatory features as possible cardiovascular markers in diabetes

    PubMed Central

    Tuttolomondo, Antonino; Maida, Carlo; Pinto, Antonio

    2015-01-01

    Diabetic foot ulcerations have been extensively reported as vascular complications of diabetes mellitus associated with a high degree of morbidity and mortality. Diabetic foot syndrome (DFS), as defined by the World Health Organization, is an “ulceration of the foot (distally from the ankle and including the ankle) associated with neuropathy and different grades of ischemia and infection”. Pathogenic events able to cause diabetic foot ulcers are multifactorial. Among the commonest causes of this pathogenic pathway it’s possible to consider peripheral neuropathy, foot deformity, abnormal foot pressures, abnormal joint mobility, trauma, peripheral artery disease. Several studies reported how diabetic patients show a higher mortality rate compared to patients without diabetes and in particular these studies under filled how cardiovascular mortality and morbidity is 2-4 times higher among patients affected by type 2 diabetes mellitus. This higher degree of cardiovascular morbidity has been explained as due to the observed higher prevalence of major cardiovascular risk factor, of asymptomatic findings of cardiovascular diseases, and of prevalence and incidence of cardiovascular and cerebrovascular events in diabetic patients with foot complications. In diabetes a fundamental pathogenic pathway of most of vascular complications has been reported as linked to a complex interplay of inflammatory, metabolic and procoagulant variables. These pathogenetic aspects have a direct interplay with an insulin resistance, subsequent obesity, diabetes, hypertension, prothrombotic state and blood lipid disorder. Involvement of inflammatory markers such as IL-6 plasma levels and resistin in diabetic subjects as reported by Tuttolomondo et al confirmed the pathogenetic issue of the a “adipo-vascular” axis that may contribute to cardiovascular risk in patients with type 2 diabetes. This “adipo-vascular axis” in patients with type 2 diabetes has been reported as characterized

  10. Peripheral blood gene expression patterns discriminate among chronic inflammatory diseases and healthy controls and identify novel targets.

    PubMed

    Mesko, Bertalan; Poliska, Szilard; Szegedi, Andrea; Szekanecz, Zoltan; Palatka, Karoly; Papp, Maria; Nagy, Laszlo

    2010-05-05

    Chronic inflammatory diseases including inflammatory bowel disease (IBD; Crohn's disease and ulcerative colitis), psoriasis and rheumatoid arthritis (RA) afflict millions of people worldwide, but their pathogenesis is still not well understood. It is also not well known if distinct changes in gene expression characterize these diseases and if these patterns can discriminate between diseased and control patients and/or stratify the disease. The main focus of our work was the identification of novel markers that overlap among the 3 diseases or discriminate them from each other. Diseased (n = 13, n = 15 and n = 12 in IBD, psoriasis and RA respectively) and healthy patients (n = 18) were recruited based on strict inclusion and exclusion criteria; peripheral blood samples were collected by clinicians (30 ml) in Venous Blood Vacuum Collection Tubes containing EDTA and peripheral blood mononuclear cells were separated by Ficoll gradient centrifugation. RNA was extracted using Trizol reagent. Gene expression data was obtained using TaqMan Low Density Array (TLDA) containing 96 genes that were selected by an algorithm and the statistical analyses were performed in Prism by using non-parametric Mann-Whitney U test (P-values < 0.05). Here we show that using a panel of 96 disease associated genes and measuring mRNA expression levels in peripheral blood derived mononuclear cells; we could identify disease-specific gene panels that separate each disease from healthy controls. In addition, a panel of five genes such as ADM, AQP9, CXCL2, IL10 and NAMPT discriminates between all samples from patients with chronic inflammation and healthy controls. We also found genes that stratify the diseases and separate different subtypes or different states of prognosis in each condition. These findings and the identification of five universal markers of chronic inflammation suggest that these diseases have a common background in pathomechanism, but still can be separated by peripheral blood

  11. Markers of endothelial damage in patients with chronic kidney disease on hemodialysis.

    PubMed

    Carmona, Andrés; Agüera, Maria L; Luna-Ruiz, Carlos; Buendía, Paula; Calleros, Laura; García-Jerez, Andrea; Rodríguez-Puyol, Manuel; Arias, Manuel; Arias-Guillen, Marta; de Arriba, Gabriel; Ballarin, Jose; Bernis, Carmen; Fernández, Elvira; García-Rebollo, Sagrario; Mancha, Javier; Del Peso, Gloria; Pérez, Estefanía; Poch, Esteban; Portolés, Jose M; Rodríguez-Puyol, Diego; Sánchez-Villanueva, Rafael; Sarro, Felipe; Torres, Armando; Martín-Malo, Alejandro; Aljama, Pedro; Ramírez, Rafael; Carracedo, Julia

    2017-04-01

    Patients with Stage 5 chronic kidney disease who are on hemodialysis (HD) remain in a chronic inflammatory state, characterized by the accumulation of uremic toxins that induce endothelial damage and cardiovascular disease (CVD). Our aim was to examine microvesicles (MVs), monocyte subpopulations, and angiopoietins (Ang) to identify prognostic markers in HD patients with or without diabetes mellitus (DM). A total of 160 prevalent HD patients from 10 centers across Spain were obtained from the Biobank of the Nephrology Renal Network (Madrid, Spain): 80 patients with DM and 80 patients without DM who were matched for clinical and demographic criteria. MVs from plasma and several monocyte subpopulations (CD14(2+)/CD16(+), CD14(+)/CD16(2+)) were analyzed by flow cytometry, and the plasma concentrations of Ang1 and Ang2 were quantified by ELISA. Data on CVD were gathered over the 5.5 yr after these samples were obtained. MV level, monocyte subpopulations (CD14(+)/CD16(2+) and CD14(2+)/CD16(+)), and Ang2-to-Ang1 ratios increased in HD patients with DM compared with non-DM patients. Moreover, MV level above the median (264 MVs/µl) was associated independently with greater mortality. MVs, monocyte subpopulations, and Ang2-to-Ang1 ratio can be used as predictors for CVD. In addition, MV level has a potential predictive value in the prevention of CVD in HD patients. These parameters undergo more extensive changes in patients with DM. Copyright © 2017 the American Physiological Society.

  12. Chronic stress induced disturbances in Laminin: a significant contributor to modulating microglial pro-inflammatory tone?

    PubMed

    Pietrogrande, Giovanni; Mabotuwana, Nishani; Zhao, Zidan; Mahmoud, Abdolhoseini; Johnson, Sarah J; Nilsson, Michael; Walker, Frederick R

    2017-09-21

    Over the last decade, evidence supporting a link between microglia enhanced neuro-inflammatory signalling and mood disturbance has continued to build. One issue that has not been well addressed yet are the factors that drive microglia to enter into a higher pro-inflammatory state. The current study addressed the potential role of the extracellular matrix protein Laminin. C57BL6 adult mice were either exposed to chronic stress or handled for 6 consecutive weeks. Changes in Laminin, microglial morphology and pro-inflammatory cytokine expression were examined in tissue obtained from mice exposed to a chronic restraint stress procedure. These in-vivo investigations were complemented by an extensive set of in-vitro experiments utilising both a primary microglia and BV2 cell line to examine how Laminin influenced microglial pro-inflammatory tone. Chronic stress was associated with enhanced the expression of Laminin, microglial de-ramification and pro-inflammatory cytokine signalling. We further identified that microglia when cultured in the presence of Laminin produced and released significantly greater levels of pro-inflammatory cytokines; took longer to return to baseline following stimulation and exhibited enhanced phagocytic activity. These results suggest that chronic restraint stress is capable of modulating Laminin within the CNS, an effect that has implications for understanding environmental mediated disturbances of microglial function. Copyright © 2017. Published by Elsevier Inc.

  13. INFLAMMATORY MARKERS ASSOCIATED WITH TRAUMA AND INFECTION IN RED-TAILED HAWKS (BUTEO JAMAICENSIS) IN THE USA.

    PubMed

    Lee, Kelly A; Goetting, Valerie S; Tell, Lisa A

    2015-10-01

    Changes in inflammatory marker concentrations or activity can be used to monitor health and disease condition of domestic animals but have not been applied with the same frequency to wildlife. We measured concentrations or activity of six inflammatory markers (ceruloplasmin, haptoglobin, mannan-binding lectin-dependent complement [MBL/complement], unsaturated iron-binding capacity (UIBC) and total iron-binding capacity (TIBC), and plasma iron) in apparently healthy and sick or injured Red-tailed Hawks (Buteo jamaicensis). Haptoglobin and ceruloplasmin activities were consistently elevated in sick or injured hawks (2.1 and 2.5 times higher, respectively), and plasma iron concentrations decreased (0.46 times lower), relative to those of healthy birds. There were no differences between healthy and unhealthy hawks in TIBC and UIBC concentrations or MBL/complement activity. Therefore, haptoglobin, ceruloplasmin, and plasma iron would be useful inclusions in a panel of inflammatory markers for monitoring health in raptors.

  14. Comparative usefulness of inflammatory markers to indicate bacterial infection-analyzed according to blood culture results and related clinical factors.

    PubMed

    Nishikawa, Hirokazu; Shirano, Michinori; Kasamatsu, Yu; Morimura, Ayumi; Iida, Ko; Kishi, Tomomi; Goto, Tetsushi; Okamoto, Saki; Ehara, Eiji

    2016-01-01

    To assess relationships of inflammatory markers and 2 related clinical factors with blood culture results, we retrospectively investigated inpatients' blood culture and blood chemistry findings that were recorded from January to December 2014 using electronic medical records and analyzed the data of 852 subjects (426 culture-positive and 426 culture-negative). Results suggested that the risk of positive blood culture statistically increased as inflammatory marker levels and the number of related factors increased. Concerning the effectiveness of inflammatory markers, when the outcome definition was also changed for C-reactive protein (CRP), the odds ratio had a similar value, whereas when the outcome definition of blood culture positivity was used for procalcitonin (PCT), the greatest effectiveness of that was detected. Therefore, the current results suggest that PCT is more useful than CRP as an auxiliary indication of bacterial infection.

  15. Clinical application of expectorant therapy in chronic inflammatory airway diseases (Review)

    PubMed Central

    ZHANG, TING; ZHOU, XIANGDONG

    2014-01-01

    Airway mucus hypersecretion is a significant clinical and pathological feature of chronic inflammatory airway diseases. Its clinical presentations include recurrent coughing and phlegm. Airway mucus is closely associated with the occurrence, development and prognosis of chronic inflammatory airway diseases and critically affects the lung function, quality of life, hospitalization rate and mortality of patients with chronic inflammatory airway diseases. Therefore, expectorant therapies targeting the potential mechanisms of mucus hypersecretion have been the focus of numerous studies. Conventional expectorants are mainly mucoactive medicines, including nausea-stimulating expectorants, mucolytics, mucokinetics, and proteases and nucleases. In addition, certain traditional Chinese herbal medicines and non-mucoactive agents, including muscarinic acetylcholine receptor antagonists, corticosteroids, leukotriene receptor antagonists and macrolide antibiotics, have also shown expectorant effects. Several novel medicines for expectorant therapy have emerged, including cholesterol-lowering statins, epidermal growth factor receptor tyrosine kinase inhibitors, phosphodiesterase-4 inhibitors, stanozolol, surfactants, flavonoids, tachykinin receptor antagonists, protease inhibitors, cytokine antagonists and purinergic agonists. With the increasing number of multidisciplinary studies, the effectiveness of expectorant therapy for the treatment of chronic inflammatory airway diseases has been confirmed. Therefore, the development of novel expectorants and the standardization of expectorant therapy are the direction and focus of future studies, thus benefiting patients who have a chronic inflammatory airway disease. PMID:24660026

  16. Reduced GABAergic transmission in the ventrobasal thalamus contributes to thermal hyperalgesia in chronic inflammatory pain

    PubMed Central

    Zhang, Chan; Chen, Rong-Xiang; Zhang, Yu; Wang, Jie; Liu, Feng-Yu; Cai, Jie; Liao, Fei-Fei; Xu, Fu-Qiang; Yi, Ming; Wan, You

    2017-01-01

    The ventrobasal (VB) thalamus is innervated by GABAergic afferents from the thalamic reticular nucleus (TRN) and participates in nociception. But how the TRN-VB pathway regulates pain is not fully understood. In the present study, we reported decreased extracellular GABA levels in the VB of rats with CFA-induced chronic inflammatory pain, measured by microdialysis with HPLC analysis. In vitro whole-cell patch-clamp recording showed decreased amplitudes of tonic currents, increased frequencies of mIPSCs, and increased paired-pulse ratios in thalamic slices from chronic inflammatory rats (7 days). Microinjection of the GABAAR agonist muscimol and optogenetic activation of the TRN-VB pathway relieved thermal hyperalgesia in chronic inflammatory pain. By contrast, microinjecting the extrasynaptic GABAAR agonist THIP or selective knockout of synaptic GABAAR γ2 subunits aggravated thermal hyperalgesia in the chronic stage of inflammatory pain. Our findings indicate that reduced GABAergic transmission in the VB contributes to thermal hyperalgesia in chronic inflammatory pain, which could be a synaptic target for pharmacotherapy. PMID:28150719

  17. Exacerbation of chronic inflammatory diseases by infectious agents: Fact or fiction?

    PubMed Central

    Wang, Cheng-Ming; Kaltenboeck, Bernhard

    2010-01-01

    Chronic inflammatory diseases caused by obesity represent critical public health concerns worldwide. In these diseases such as metabolic syndrome, diabetes and atherosclerosis, adipose tissue acts as an endocrine organ that releases large quantities of inflammatory mediators into circulation. Besides classically recognized effectors on the development of obesity and resultant conditions, infection has attracted attention as an enhancer of chronic inflammatory diseases. Infectious diseases have long been associated with obesity, metabolic syndrome, diabetes and atherosclerosis. However, the infectious hypothesis for chronic inflammatory diseases has been challenged by inconclusive clinical trials. Nevertheless, the large body of evidence accumulated over decades on the association of infectious diseases with obesity, diabetes and cardiovascular disease should not be disregarded. Instead, re-formulation of hypotheses of the mechanisms by which microbes affect obesity-associated diseases may be required with an emphasis on the early events in the progression of such diseases and the multifactorial nature of pathogen-host interactions. This review focuses on pathogens that directly promote obesity and on pathogens that cause chronic infections and thereby enhance metabolic diseases in obese patients. A new perspective on the interaction between infections and obesity-related diseases may improve management of chronic inflammatory diseases that rank high among global threats to human health. PMID:21537425

  18. Diagnostic value of sonography in treatment-naive chronic inflammatory neuropathies.

    PubMed

    Goedee, H Stephan; van der Pol, W Ludo; van Asseldonk, Jan-Thies H; Franssen, Hessel; Notermans, Nicolette C; Vrancken, Alexander J F E; van Es, Michael A; Nikolakopoulos, Stavros; Visser, Leo H; van den Berg, Leonard H

    2017-01-10

    To determine the diagnostic value of high-resolution ultrasound (HRUS) for detection of chronic inflammatory demyelinating polyneuropathy (CIDP), Lewis-Sumner syndrome (LSS), and multifocal motor neuropathy (MMN). Between January 2013 and January 2015, we enrolled 75 consecutive treatment-naive patients with chronic inflammatory neuropathies and 70 disease controls. We performed extensive nerve conduction and standardized HRUS studies bilaterally of large arm and leg nerves and brachial plexus. We determined optimal sonographic cutoff values of nerve size and used receiver operating characteristic analysis and logistic regression models to identify nerve combinations with optimal diagnostic performance. Enlargement of median nerve at forearm >10 mm(2), upper arm >13 mm(2), and any trunk of brachial plexus >8 mm(2) was 99% specific for chronic inflammatory neuropathies. A shortened HRUS protocol for detecting this abnormal nerve enlargement showed high sensitivity (83%-95%), positive predictive value (100%), and negative predictive value (98%) in discriminating CIDP, LSS, and MMN from clinical mimics. Sonographic enlargement of proximal median nerve segments in the arms and brachial plexus is a key feature of chronic inflammatory neuropathies, which helps to reliably distinguish them from axonal neuropathies and amyotrophic lateral sclerosis. This study provides Class II evidence that, in absence of clinical features that suggest a hereditary demyelinating neuropathy, sonographic enlargement of proximal median nerve segments and brachial plexus accurately identifies patients with chronic inflammatory neuropathies. © 2016 American Academy of Neurology.

  19. Inflammatory markers in blood and serum tumor markers predict survival in patients with epithelial appendiceal neoplasms undergoing surgical cytoreduction and intraperitoneal chemotherapy.

    PubMed

    Chua, Terence C; Chong, Chanel H; Liauw, Winston; Zhao, Jing; Morris, David L

    2012-08-01

    The study examines the role inflammatory and tumor markers as biomarkers to preoperatively predict outcome in patients with epithelial appendiceal neoplasm undergoing cytoreduction and intraperitoneal chemotherapy. Associations between baseline variables, tumor markers [CEA (carcinoembyronic antigen], CA125, CA199), inflammatory markers including neutrophils-lymphocyte ratio (NLR), platelet-lymphocyte ratio (PLR), and C-reactive protein (CRP) with progression-free survival (PFS) and overall survival (OS) were examined in patients undergoing surgical cytoreduction and intraperitoneal chemotherapy for epithelial appendiceal neoplasm. A total of 174 patients with epithelial appendiceal neoplasm (low-grade pseudomyxoma, n = 117; appendiceal cancer, n = 57) underwent cytoreduction. On univariate analysis, all 3 inflammatory and tumor markers predicted for both PFS and OS, respectively; NLR ≤ 2.6 (P = 0.01, P = 0.002), PLR ≤ 166 (P = 0.006, P = 0.016), CRP ≤ 12.5 (P = 0.001, P = 0.008), CEA (P < 0.001, P = 0.001), CA125 (P = 0.004, P < 0.001), CA199 (P < 0.001, P < 0.001). On multivariate analysis, there were no independent predictors of OS. PFS was independently associated with the presence of lymph node metastasis (P = 0.02), CA199 > 37 (P = 0.003), and a CRP > 12.5 (P = 0.013). A higher peritoneal cancer index (PCI > 24) was associated with elevation in CEA > 12, CA125 > 39, CA199 > 37, PLR > 166 and CRP > 12. The tumor histologic subtype was associated with CA 199 levels. The results from this investigation suggest that preoperative inflammatory markers in blood and serologic tumor markers may predict outcomes and are associated with tumor biology in patients with epithelial appendiceal neoplasm undergoing cytoreduction and intraperitoneal chemotherapy treatment.

  20. Urinary leukotriene E4 concentrations as a potential marker of inflammation in dogs with inflammatory bowel disease.

    PubMed

    Im Hof, M; Schnyder, M; Hartnack, S; Stanke-Labesque, F; Luckschander, N; Burgener, I A

    2012-01-01

    Inflammatory bowel disease (IBD) and food-responsive diarrhea (FRD) are chronic enteropathies of dogs (CCE) that currently can only be differentiated by their response to treatment after exclusion of other diseases. In humans, increased urinary concentrations of leukotriene E4 (LTE4) have been associated with active IBD. To evaluate urinary LTE4 concentrations in dogs with IBD, FRD, and healthy controls, and to assess correlation of urinary LTE4 concentrations with the canine IBD activity index (CIBDAI) scores. Eighteen dogs with IBD, 19 dogs with FRD, and 23 healthy control dogs. In this prospective study, urine was collected and CIBDAI scores were calculated in client-owned dogs with IBD and those with FRD. Quantification of LTE4 in urine was performed by liquid chromatography-tandem mass spectrometry and corrected to creatinine. Urinary LTE4 concentrations were highest in dogs with IBD (median 85.2 pg/mg creatinine [10th-90th percentiles 10.9-372.6]) followed by those with FRD (median 31.2 pg/mg creatinine [10th-90th percentiles 6.2-114.5]) and control dogs (median 21.1 pg/mg creatinine [10th-90th percentiles 9.1-86.5]). Urinary LTE4 concentrations were higher in dogs with IBD than in control dogs (P = .011), but no significant difference between IBD and FRD was found. No correlation was found between urinary LTE4 concentrations and CIBDAI. The higher urinary LTE4 concentrations in dogs with IBD suggest that cysteinyl leukotriene pathway activation might be a component of the inflammatory process in canine IBD. Furthermore, urinary LTE4 concentrations are of potential use as a marker of inflammation in dogs with CCE. Copyright © 2012 by the American College of Veterinary Internal Medicine.

  1. Dietary antioxidant and anti-inflammatory intake modifies the effect of cadmium exposure on markers of systemic inflammation and oxidative stress

    SciTech Connect

    Colacino, Justin A.; Arthur, Anna E.; Ferguson, Kelly K.; Rozek, Laura S.

    2014-05-01

    Chronic cadmium exposure may cause disease through induction of systemic oxidative stress and inflammation. Factors that mitigate cadmium toxicity and could serve as interventions in exposed populations have not been well characterized. We used data from the 2003–2010 National Health and Nutrition Examination Survey to quantify diet's role in modifying associations between cadmium exposure and oxidative stress and inflammation. We created a composite antioxidant and anti-inflammatory diet score (ADS) by ranking participants by quintile of intake across a panel of 19 nutrients. We identified associations and effect modification between ADS, urinary cadmium, and markers of oxidative stress and inflammation by multiple linear regression. An interquartile range increase in urinary cadmium was associated with a 47.5%, 8.8%, and 3.7% increase in C-reactive protein (CRP), gamma glutamyl transferase (GGT), and alkaline phosphatase (ALP), respectively. An interquartile range increase in ADS was associated with an 7.4%, 3.3%, 5.2%, and 2.5% decrease in CRP, GGT, ALP, and total white blood cell count respectively, and a 3.0% increase in serum bilirubin. ADS significantly attenuated the association between cadmium exposure, CRP and ALP. Dietary interventions may provide a route to reduce the impact of cadmium toxicity on the population level. - Highlights: • Cadmium may cause chronic disease through oxidative stress or inflammation. • We developed a score to quantify dietary antioxidant and anti-inflammatory intake. • Cadmium was associated with markers of oxidative stress and inflammation. • Antioxidant and anti-inflammatory intake mitigated the effects of cadmium exposure. • Dietary interventions may be effective against chronic cadmium toxicity.

  2. Reduction of chronic abdominal pain in patients with inflammatory bowel disease through transcranial direct current stimulation: a randomized controlled trial.

    PubMed

    Volz, Magdalena S; Farmer, Annabelle; Siegmund, Britta

    2016-02-01

    Inflammatory bowel disease (IBD) is frequently associated with chronic abdominal pain (CAP). Transcranial direct current stimulation (tDCS) has been proven to reduce chronic pain. This study aimed to investigate the effects of tDCS in patients with CAP due to IBD. This randomized, sham-controlled, double blind, parallel-designed study included 20 patients with either Crohn disease or ulcerative colitis with CAP (≥3/10 on the visual analog scale (VAS) in 3/6 months). Anodal or sham tDCS was applied over the primary motor cortex for 5 consecutive days (2 mA, 20 minutes). Assessments included VAS, pressure pain threshold, inflammatory markers, and questionnaires on quality of life, functional and disease specific symptoms (Irritable Bowel Syndrome-Severity Scoring System [IBS-SSS]), disease activity, and pain catastrophizing. Follow-up data were collected 1 week after the end of the stimulation. Statistical analyses were performed using analysis of variance and t tests. There was a significant reduction of abdominal pain in the anodal tDCS group compared with sham tDCS. This effect was evident in changes in VAS and pressure pain threshold on the left and right sides of the abdomen. In addition, 1 week after stimulation, pain reduction remained significantly decreased in the right side of the abdomen. There was also a significant reduction in scores on pain catastrophizing and on IBS-SSS when comparing both groups. Inflammatory markers and disease activity did not differ significantly between groups throughout the experiment. Transcranial direct current stimulation proved to be an effective and clinically relevant therapeutic strategy for CAP in IBD. The analgesic effects observed are unrelated to inflammation and disease activity, which emphasizes central pain mechanisms in CAP.

  3. Inflammatory markers as predictors of postoperative adverse outcome in octogenarian surgical patients: an observational prospective study.

    PubMed

    González-Martínez, Sergio; Olona Tabueña, Noemí; Martín Baranera, Montserrat; Martí-Saurí, Isidro; Moll, Josep Lluís; Morales García, Miguel Ángel; Borrell Grau, Nuria; Pueyo Zurdo, José María

    2015-03-01

    The value of inflammatory proteins, interleukin-6 and alpha-1-acid glycoprotein as prognostic factors in elderly people undergoing surgery has not been determined yet. To know whether preoperatively determined inflammatory markers may predict the postoperative outcome of elderly patients undergoing surgery. A scoring system for predicting postoperative morbidity was assessed. Hospital-based observational prospective study, with geriatric surgical patients. Preoperative determination of following data: age, gender, scheduled or urgent operation, comorbid diseases, malignancy, physical, mental and nutritional profile. Biochemical markers of inflammation, C Reactive Protein, interleukin-6, and alpha-1-acid glycoprotein were also studied. Preoperative data and postoperative complications were recorded. Binary logistic regression analysis was used to obtain a morbidity risk prediction model. A total of 225 patients were included. Fifty-five patients (24.4%) had postoperative complications, with a mortality rate of 5.3%. Binary logistic regression analysis showed an independent relation between morbidity and the variables malignancy, alpha-1-acid glycoprotein and interleukin-6. The risk (R) of postoperative morbidity adjusted by age was calculated. The model showed a 22.2% sensitivity, 94.8% specificity, and a percentage of correct classification of 78.3%. The area under the ROC curve was 0.781 (95% CI: 0.703-0.858). An age-adjusted equation for predicting 30-day morbidity that included malignancy, serum IL-6 and alpha 1-acid glycoprotein levels may be useful for risk assessment in octogenarian surgical patients. Copyright © 2014 AEC. Publicado por Elsevier España, S.L.U. All rights reserved.

  4. Expression of Vascular Notch Ligand Delta-Like 4 and Inflammatory Markers in Breast Cancer

    PubMed Central

    Jubb, Adrian M.; Soilleux, Elizabeth J.; Turley, Helen; Steers, Graham; Parker, Andrew; Low, Irene; Blades, Jennifer; Li, Ji-Liang; Allen, Paul; Leek, Russell; Noguera-Troise, Irene; Gatter, Kevin C.; Thurston, Gavin; Harris, Adrian L.

    2010-01-01

    Delta-like ligand 4 (Dll4) is a Notch ligand that is predominantly expressed in the endothelium. Evidence from xenografts suggests that inhibiting Dll4 may overcome resistance to antivascular endothelial growth factor therapy. The aims of this study were to characterize the expression of Dll4 in breast cancer and assess whether it is associated with inflammatory markers and prognosis. We examined 296 breast adenocarcinomas and 38 ductal carcinoma in situ tissues that were represented in tissue microarrays. Additional whole sections representing 10 breast adenocarcinomas, 10 normal breast tissues, and 16 angiosarcomas were included. Immunohistochemistry was then performed by using validated antibodies against Dll4, CD68, CD14, Dendritic Cell-Specific Intercellular adhesion molecule-3-Grabbing Non-integrin (DC-SIGN), CD123, neutrophil elastase, CD31, and carbonic anhydrase 9. Dll4 was selectively expressed by intratumoral endothelial cells in 73% to 100% of breast adenocarcinomas, 18% of in situ ductal carcinomas, and all lactating breast cases, but not normal nonlactating breast. High intensity of endothelial Dll4 expression was a statistically significant adverse prognostic factor in univariate (P = 0.002 and P = 0.01) and multivariate analyses (P = 0.03 and P = 0.04) of overall survival and relapse-free survival, respectively. Among the inflammatory markers, only CD68 and DC-SIGN were significant prognostic factors in univariate (but not multivariate) analyses of overall survival (P = 0.01 and 0.002, respectively). In summary, Dll4 was expressed by endothelium associated with breast cancer cells. In these retrospective subset analyses, endothelial Dll4 expression was a statistically significant multivariate prognostic factor. PMID:20167860

  5. Cardiac Dysfunction in Association with Increased Inflammatory Markers in Primary Aldosteronism

    PubMed Central

    Lim, Jung Soo; Park, Sungha; Park, Sung Il; Oh, Young Taik; Choi, Eunhee; Kim, Jang Young

    2016-01-01

    Background Oxidative stress in primary aldosteronism (PA) is thought to worsen aldosterone-induced damage by activating proinflammatory processes. Therefore, we investigated whether inflammatory markers associated with oxidative stress is increased with negative impacts on heart function as evaluated by echocardiography in patients with PA. Methods Thirty-two subjects (mean age, 50.3±11.0 years; 14 males, 18 females) whose aldosterone-renin ratio was more than 30 among patients who visited Severance Hospital since 2010 were enrolled. Interleukin-1β (IL-1β), IL-6, IL-8, monocyte chemoattractant protein 1, tumor necrosis factor α (TNF-α), and matrix metalloproteinase 2 (MMP-2), and MMP-9 were measured. All patients underwent adrenal venous sampling with complete access to both adrenal veins. Results Only MMP-2 level was significantly higher in the aldosterone-producing adenoma (APA) group than in the bilateral adrenal hyperplasia (BAH). Patients with APA had significantly higher left ventricular (LV) mass and A velocity, compared to those with BAH. IL-1β was positively correlated with left atrial volume index. Both TNF-α and MMP-2 also had positive linear correlation with A velocity. Furthermore, MMP-9 showed a positive correlation with LV mass, whereas it was negatively correlated with LV end-systolic diameter. Conclusion These results suggest the possibility that some of inflammatory markers related to oxidative stress may be involved in developing diastolic dysfunction accompanied by LV hypertrophy in PA. Further investigations are needed to clarify the role of oxidative stress in the course of cardiac remodeling. PMID:27834080

  6. Dialysis modality and nutritional status are associated with variability of inflammatory markers.

    PubMed

    Snaedal, Sunna; Qureshi, Abdul R; Lund, Sigrún H; Germanis, Guna; Hylander, Britta; Heimbürger, Olof; Carrero, Juan J; Stenvinkel, Peter; Bárány, Peter

    2016-08-01

    Inflammation is a common feature in dialysis patients and is associated with cardiovascular complications and poor outcome. Measuring the variability of inflammatory markers may help in understanding underlying factors triggering inflammation. Whether the inflammatory pattern in hemodialysis (HD) and peritoneal dialysis (PD) patients differs has scarcely been studied. Here we explored factors associated with the magnitude and variability of inflammation markers in HD and PD patients. In two 3-month, prospective cohort studies comprising 228 prevalent HD and 80 prevalent PD patients, interleukin-6 (IL-6) and high-sensitivity C-reactive protein (CRP) were measured in blood samples drawn each month and every week, respectively. Information on comorbidity, protein-energy wasting (PEW) and medications was gathered at baseline, and information on symptoms potentially related to inflammation was gathered weekly. A mixed-effect model was used for multivariate analysis of factors linked to CRP and IL-6 variation. IL-6 and CRP levels were higher and showed higher variability in HD versus PD patients [median IL-6 8.3 (interquartile range, IQR, 5.3-14.5) versus 6.7 (IQR 4.2-10.0) pg/mL, P < 0.001 and median CRP 6.1 (IQR 2.5-14.0) versus 5.4 (IQR 1.6-9.0) mg/L, P < 0.001). PEW predicted increased inflammation variability after correcting for age, sex, dialysis vintage, modality and comorbidity. Increased comorbidity predicted IL-6, but not CRP, variability. Circulating concentrations as well as variability of IL-6 and CRP levels were higher in HD as compared with PD patients. In HD and PD patients, short-term variability of IL-6 and CRP levels associated strongly with PEW, while comorbidity was related to IL-6 but not to CRP variability. © The Author 2016. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved.

  7. Combined Serological, Genetic, and Inflammatory Markers Differentiate Non-IBD, Crohn’s Disease, and Ulcerative Colitis Patients

    PubMed Central

    Plevy, Scott; Silverberg, Mark S.; Lockton, Steve; Stockfisch, Tom; Croner, Lisa; Stachelski, Jordan; Brown, Michelle; Triggs, Cheryl; Chuang, Emil; Princen, Fred; Singh, Sharat

    2013-01-01

    Background Previous studies have demonstrated that serological markers can assist in diagnosing inflammatory bowel disease (IBD). In this study, we aim to build a diagnostic tool incorporating serological markers, genetic variants, and markers of inflammation into a computational algorithm to examine patterns of combinations of markers to (1) identify patients with IBD and (2) differentiate patients with Crohn’s disease (CD) from ulcerative colitis (UC). Methods In this cross-sectional study, patient blood samples from 572 CD, 328 UC, 437 non-IBD controls, and 183 healthy controls from academic and community centers were analyzed for 17 markers: 8 serological markers (ASCA-IgA, ASCA-IgG, ANCA, pANCA, OmpC, CBir1, A4-Fla2, and FlaX), 4 genetic markers (ATG16L1, NKX2-3, ECM1, and STAT3), and 5 inflammatory markers (CRP, SAA, ICAM-1, VCAM-1, and VEGF). A diagnostic Random Forest algorithm was constructed to classify IBD, CD, and UC. Results Receiver operating characteristic analysis compared the diagnostic accuracy of using a panel of serological markers only (ASCA-IgA, ASCA-IgG, ANCA, pANCA, OmpC, and CBir1) versus using a marker panel that in addition to the serological markers mentioned above also included gene variants, inflammatory markers, and 2 additional serological markers (A4-Fla2 and FlaX). The extended marker panel increased the IBD versus non-IBD discrimination area under the curve from 0.80 (95% confidence interval [CI], ±0.05) to 0.87 (95% CI, ±0.04; P < 0.001). The CD versus UC discrimination increased from 0.78 (95% CI, ±0.06) to 0.93 (95% CI, ±0.04; P < 0.001). Conclusions Incorporating a combination of serological, genetic, and inflammation markers into a diagnostic algorithm improved the accuracy of identifying IBD and differentiating CD from UC versus using serological markers alone. PMID:23518807

  8. Hyperosmolarity and Benzalkonium Chloride Differently Stimulate Inflammatory Markers in Conjunctiva-Derived Epithelial Cells in vitro.

    PubMed

    Warcoin, Elise; Clouzeau, Chloé; Roubeix, Christophe; Raveu, Anne-Laure; Godefroy, David; Riancho, Luisa; Baudouin, Christophe; Brignole-Baudouin, Françoise

    2016-12-10

    Tear hyperosmolarity is known to cause ocular surface inflammation in dry eye syndrome. Benzalkonium chloride (BAK), an eyedrop preservative, is known to induce dry eye in long-term-treated patients. Analyzing the modulation of the proinflammatory potential of hyperosmolarity in the presence of BAK on the conjunctiva could give new insights into the effect of this preservative on the disease. In a hyperosmolar model on a conjunctiva-derived cell line, and in the presence of BAK, we evaluated key inflammatory markers [CCL2, IL-8, IL-6, macrophage migration inhibitory factor (MIF) and intercellular adhesion molecule (ICAM)-1] as well as the osmoprotectant element nuclear factor of activated T cells (NFAT)5 using ELISA, RT-qPCR or immunofluorescence staining. Hyperosmolarity highly stimulated CCL2 and NFAT5 in these cells. BAK alone only increased IL-6 expression. The stress-combined condition stimulated CCL2, NFAT5, MIF and IL-8 secretion. ICAM-1 was not modulated by any of the conditions tested. In this model, hyperosmolarity and BAK induced the release of different proinflammatory mediators, and, when combined, they lead to the release of additional inflammatory cytokines. This in vitro study highlights the importance of avoiding long-term ophthalmic treatments containing BAK, as tear film hyperosmolarity can be a result of its detergent action.

  9. Serum inflammatory markers in the elderly: are they useful in differentiating sepsis from SIRS?

    PubMed

    Talebi-Taher, Mahshid; Babazadeh, Shahin; Barati, Mitra; Latifnia, Maryam

    2014-01-01

    Differentiating sepsis from other noninfectious causes of systemic inflammation is often difficult in the elderly. The aim of this study was to evaluate the ability of C-reactive protein (CRP), Erythrocyte Sedimentation Rate (ESR), procalcitonin (PCT), and Interleukin-6 (IL-6) to identify elderly patients with sepsis. In this single center prospective observational study, we included all consecutive elderly patients admitted with suspected sepsis and systemic inflammatory response syndrome (SIRS) in an emergency department. Blood samples for measuring CRP, PCT, IL-6, ESR and white blood cells (WBC) count were taken at first day of admission. Sensitivity, specificity, positive and negative predictive values were calculated for each inflammatory markers being studied. A total of 150 elderly patients aged 65 and older, 50 with sepsis and 50 with SIRS, and fifty individuals in a normal health status were included. CRP exhibited the greatest sensitivity (98%) and negative predictive value (98.6%) and performed best in differentiating patients with sepsis from those with SIRS. In a receiver operating characteristic curve analysis, IL-6 performed best in distinguishing between SIRS and the control group (AUC 0.75, 95% CI). On the other hand, both CRP and ESR appeared to be a more accurate diagnostic parameter for differentiating sepsis from SIRS among elderly patients.

  10. Cholinesterases as markers of the inflammatory process associated oxidative stress in cattle infected by Babesia bigemina.

    PubMed

    Doyle, Rovaina L; Da Silva, Aleksandro S; Oliveira, Camila B; França, Raqueli T; Carvalho, Fabiano B; Abdalla, Fátima H; Costa, Pauline; Klafke, Guilherme M; Martins, João R; Tonin, Alexandre A; Castro, Verônica S P; Santos, Franklin G B; Lopes, Sonia T A; Andrade, Cinthia M

    2016-06-01

    The objective of this study was to assess the influence of an asymptomatic experimental infection by Babesia bigemina on cholinesterase's as markers of the inflammatory process and biomarkers of oxidative imbalance. For this purpose, eight naive animals were used, as follows: four as controls or uninfected; and four infected with an attenuated strain of B. bigemina. Blood samples were collected on days 0, 7 and 11 post-inoculation (PI). Parasitemia was determined by blood smear evaluation, showing that the infection by B. bigemina resulted in mean 0.725 and 0.025% on day 7 and 11 PI, respectively, as well as mild anemia. The activities of acetylcholinesterase, butyrylcholinesterase and catalase were lower, while levels of thiobarbituric acid reactive substances and superoxide dismutase activity were higher in infected animals, when compared with the control group. This attenuated strain of B. bigemina induced an oxidative stress condition, as well as it reduces the cholinesterasés activity in infected and asymptomatic cattle. Therefore, this decrease of cholinesterase in infection by B. bigemina purpose is to inhibit inflammation, for thereby increasing acetylcholine levels, potent anti-inflammatory molecules. Copyright © 2016. Published by Elsevier Ltd.

  11. Expression of inflammatory markers in a genetic rodent model of depression.

    PubMed

    Strenn, Nina; Suchankova, Petra; Nilsson, Staffan; Fischer, Christina; Wegener, Gregers; Mathé, Aleksander A; Ekman, Agneta

    2015-03-15

    The complex bidirectional communication between the central nervous system and the peripheral immune system is of possible relevance for both normal brain functions and the development of psychiatric disorders. The aim of this investigation was to study central expression of inflammatory markers in a genetic rat model of depression (the Flinders sensitive line (FSL) and its control, the Flinders resistant line (FRL)). A peripheral immune activation was induced by lipopolysaccharide (LPS) in order to investigate possible differences in immune reactions between the two rat lines. To confirm behavioural differences between the rat lines the forced swim test was performed, a test to assess depressive-like behaviour. Expression of candidate inflammatory genes was measured in amygdala, hippocampus, hypothalamus, prefrontal cortex and striatum using quantitative real time PCR. Our results show, for the first time, significantly lower central expression of the glial-specific protein S100B and complement factor C3 in several brain regions of the FSL rats compared to controls, both at baseline and after peripheral immune stimulation. No significant differences in immune responses to LPS were observed between the rats lines. Both S100B and C3 have been suggested to be of relevance for brain development and plasticity as well as brain disorders. These proteins may be of importance for the behavioural differences between the FSL and FRL rats, and this model may be useful in studies exploring the influence of the immune system on brain functions. Copyright © 2014 Elsevier B.V. All rights reserved.

  12. Dermal microdialysis of inflammatory markers induced by aliphatic hydrocarbons in rats

    PubMed Central

    Patlolla, Ram R.; Mallampati, Ramya; Fulzele, Suniket V.; Babu, R. Jayachandra; Singh, Mandip

    2010-01-01

    In the present study we made an attempt to understand the skin irritation cascade of selected aliphatic hydrocarbons using microdialysis technique. Microdialysis probes were inserted into dermis in the dorsal skin of hairless rats. After 2 h of probes insertion, occlusive dermal exposure (2 h) was carried out with 230 μl of nonane, dodecane and tetradecane, using Hill top chambers®. Inflammatory biomarkers such as substance P (SP), α-melanocyte stimulating hormone (α-MSH) Interleukin 6 (IL-6) and prostaglandin E2 (PGE2) were analyzed in the dialysis samples by enzyme immunoassay (EIA). SP, α-MSH and IL6 were released in significant amounts following the dermal exposure of nonane and dodecane, whereas tetradecane did not induce any of these markers in significant amounts compared to control. Nonane increased the PGE2 levels in significant amounts within 2 h of chemical exposure compared to dodecane and tetradecane. IL-6 response was found to be slow and 2–3-fold increase in IL-6 levels was observed after 5 h following nonane and dodecane application. The magnitude of skin irritation exerted by all three chemicals was in the order of nonane ≥ dodecane ≥ tetradecane. The results demonstrate that microdialysis can be used to measure the inflammatory biomarkers in the skin irritation studies and irritation response of chemicals was quantifiable by this method. In conclusion, microdialysis was found to be an excellent tool to measure several inflammatory biomarkers as a function of time after dermal exposures with irritant chemicals. PMID:19152832

  13. Inflammatory fatigue and sickness behaviour - lessons for the diagnosis and management of chronic fatigue syndrome.

    PubMed

    Arnett, S V; Clark, I A

    2012-12-10

    Persistent and severe fatigue is a common part of the presentation of a diverse range of disease processes. There is a growing body of evidence indicating a common inflammatory pathophysiology underlying many conditions where fatigue is a primary patient concern, including chronic fatigue syndrome. This review explores current models of how inflammatory mediators act on the central nervous system to produce fatigue and sickness behaviour, and the commonality of these processes in conditions as diverse as surgical trauma, infection, various cancers, inflammatory bowel disease, connective tissue diseases and autoimmune diseases. We also discuss evidence indicating chronic fatigue syndrome may have important pathophysiological similarities with cytokine mediated sickness behaviour, and what lessons can be applied from sickness behaviour to chronic fatigue syndrome with regards to the diagnosis and management.

  14. Contactin 1 IgG4 associates to chronic inflammatory demyelinating polyneuropathy with sensory ataxia.

    PubMed

    Miura, Yumako; Devaux, Jérôme J; Fukami, Yuki; Manso, Constance; Belghazi, Maya; Wong, Anna Hiu Yi; Yuki, Nobuhiro

    2015-06-01

    A Spanish group recently reported that four patients with chronic inflammatory demyelinating polyneuropathy carrying IgG4 autoantibodies against contactin 1 showed aggressive symptom onset and poor response to intravenous immunoglobulin. We aimed to describe the clinical and serological features of Japanese chronic inflammatory demyelinating polyneuropathy patients displaying the anti-contactin 1 antibodies. Thirteen of 533 (2.4%) patients with chronic inflammatory demyelinating polyneuropathy had anti-contactin 1 IgG4 whereas neither patients from disease or normal control subjects did (P = 0.02). Three of 13 (23%) patients showed subacute symptom onset, but all of the patients presented with sensory ataxia. Six of 10 (60%) anti-contactin 1 antibody-positive patients had poor response to intravenous immunoglobulin, whereas 8 of 11 (73%) antibody-positive patients had good response to corticosteroids. Anti-contactin 1 IgG4 antibodies are a possible biomarker to guide treatment option.

  15. The contribution of natural selection to present-day susceptibility to chronic inflammatory and autoimmune disease

    PubMed Central

    Brinkworth, Jessica F; Barreiro, Luis B

    2015-01-01

    Chronic inflammatory and autoimmune diseases have been the focus of many genome-wide association studies (GWAS) because they represent a significant cause of illness and morbidity, and many are heritable. Almost a decade of GWAS studies suggests that the pathological inflammation associated with these diseases is controlled by a limited number of networked immune system genes. Chronic inflammatory and autoimmune diseases are enigmatic from an evolutionary perspective because they exert a negative affect on reproductive fitness. The persistence of these conditions may be partially explained by the important roles the implicated immune genes play in pathogen defense and other functions thought to be under strong natural selection in humans. The evolutionary reasons for chronic inflammatory and autoimmune disease persistence and uneven distribution across populations are the focus of this review. PMID:25458997

  16. Clinicopathologic correlations of renal microthrombosis and inflammatory markers in proliferative lupus nephritis

    PubMed Central

    2012-01-01

    Introduction Microthrombosis is often observed in lupus nephritis (LN) lesions, but its clinical significance is unknown. We evaluated the clinicopathologic correlations of renal microthrombosis and inflammatory markers in LN. Methods Kidney biopsies from 58 patients with systemic lupus erythematosus (SLE) proliferative nephritis were analyzed with immunohistochemistry (IHC) for intravascular platelet aggregates (CD61), macrophagic infiltration (CD68), and activated complement deposition (C4d). Clinical data at the time of kidney biopsy and follow-up were analyzed with regard to pathologic IHC data. Results Microthrombosis was present in 52% of the tissues. It was significantly more prevalent in patients with antiphospholipid antibodies (aPLs) (62% versus 42%). The presence of microthrombosis significantly correlated with higher macrophagic infiltration. Macrophagic infiltration but not microthrombosis was significantly correlated with C4d deposition. Only macrophagic infiltration showed a correlation with SLE and renal activity (proteinuria and active sediment), whereas neither the presence of CD61+ microthrombi nor the extent of C4d deposition correlated with LN severity or outcome. Conclusions Microthrombosis is associated with higher macrophagic infiltration in LN but does not seem to increase independently the severity of renal damage. Macrophagic infiltration was the best marker of SLE and renal activity in this LN series. PMID:22640796

  17. Health-related quality of life in chronic inflammatory neuropathies: a systematic review.

    PubMed

    Rajabally, Yusuf A; Cavanna, Andrea E

    2015-01-15

    Chronic inflammatory neuropathies represent a heterogeneous group of disorders which affect patients' functional status and quality of life. We conducted a systematic review of the scientific literature on the effects of both disease and treatment interventions on health-related quality of life (HRQoL) in this patient population. The available data are limited, as few studies have systematically considered HRQoL in patients with inflammatory neuropathies. Moreover, in treatment trials, HRQoL measures have exclusively been used as secondary outcome measures. There is some evidence suggesting that baseline pre-treatment HRQoL reports are lower in patients with chronic inflammatory neuropathy than in age and gender-matched controls. Following treatment interventions, improvements in self-reported measures were consistently documented in the physical domain of HRQoL, which in turn correlated with improvements in traditional strength and functional scales. The impact of available treatments on the quality of life of patients with inflammatory neuropathies remains largely under-investigated. Interestingly, recent, although limited evidence from generic HRQoL measures may partly or completely contradict the results found with the primary, traditional outcome measures used (rituximab for anti-MAG neuropathy; immunoglobulins versus corticosteroids for chronic inflammatory demyelinating polyneuropathy). Similarly, HRQoL measures may suggest superiority, rather than equivalence, of certain drug administration methods (subcutaneous over intravenous immunoglobulins). Further research is needed to assess HRQOL in patients with untreated chronic inflammatory neuropathies in comparison to normative values, as well as precisely quantify treatment benefit. The role of both generic and disease-specific HRQoL measures in the evaluation of patients with chronic inflammatory neuropathies is also worthy of further consideration. Crown Copyright © 2014. Published by Elsevier B.V. All

  18. Association of chronic rhinosinusitis with nasal polyps and asthma: clinical and radiological features, allergy and inflammation markers.

    PubMed

    Staikūniene, Jūrate; Vaitkus, Saulius; Japertiene, Lidija Marija; Ryskiene, Silvija

    2008-01-01

    Chronic rhinosinusitis (CRS) with and without nasal polyps represent different stages of one chronic inflammatory disease of the mucosa of the nasal cavity and paranasal sinuses. Coexistence of chronic rhinosinusitis with nasal polyps and asthma and rather similar characteristics of inflammation support assumption that chronic rhinosinusitis and nasal polyps and asthma may be, at least in part, the same disease process. We therefore aimed to evaluate the differences of sinus radiologic findings, systemic inflammation and allergy markers, pulmonary function of chronic rhinosinusitis associated with nasal polyps and asthma. A total of 121 patients with chronic rhinosinusitis referred to tertiary center were evaluated; 23 healthy persons served as controls. Sinus CT scans and nasal endoscopy were performed. Allergic rhinitis was diagnosed according to history and positive skin prick tests to common inhalant allergens. Asthma was diagnosed according to GINA by history and pulmonary function tests. Aspirin intolerance was assessed by history. Total IgE, Aspergillus fumigatus-specific IgE levels, leukocyte and eosinophil count in the peripheral blood were measured. Nasal polyps were detected in 84 patients (69.4%), asthma diagnosed in 48 patients (39.6%), associated with nasal polyps (91.7%) and allergic rhinitis in 45.5% of patients. Forty-four patients with chronic rhinosinusitis and having nasal polyps and asthma were characterized by older age (P<0.01), greater duration of nasal symptoms (P<0.001), higher number previous surgeries (P<0.01), more severe sinus disease on CT scan (P<0.001), greater blood leukocyte and eosinophil count, total IgE level (P<0.01), bronchial obstruction (P<0.05), incidence of allergic rhinitis (P<0.01), and sensitivity to house dust mite D. pteronyssinus (47.7%, P<0.01) and mold allergens (29.5%, P<0.01) comparing to the patients with isolated chronic rhinosinusitis. The extent of sinus CT changes was greater in asthmatics and correlated

  19. The role of antimicrobial peptides in chronic inflammatory skin diseases

    PubMed Central

    Majewski, Sławomir

    2016-01-01

    Antimicrobial peptides (AMPs) are effector molecules of the innate immune system of the skin. They present an activity against a broad spectrum of Gram-positive and Gram-negative bacteria as well as some fungi, parasites and enveloped viruses. Several inflammatory skin diseases including psoriasis, atopic dermatitis, acne vulgaris and rosacea are characterized by a dysregulated expression of AMPs. Antimicrobial peptides are excessively produced in lesional psoriatic scales or rosacea in contrast to the atopic skin that shows lower AMP levels when compared with psoriasis. The importance of the AMPs contribution to host immunity is indisputable as alterations in the antimicrobial peptide expression have been associated with various pathologic processes. This review discusses the biology and clinical relevance of antimicrobial peptides expressed in the skin and their role in the pathogenesis of inflammatory skin diseases. PMID:26985172

  20. Natural Killer Cells in the Orchestration of Chronic Inflammatory Diseases

    PubMed Central

    Bassani, Barbara; Tremolati, Marco; Gini, Elisabetta; Farronato, Giampietro; Bruno, Antonino

    2017-01-01

    Inflammation, altered immune cell phenotype, and functions are key features shared by diverse chronic diseases, including cardiovascular, neurodegenerative diseases, diabetes, metabolic syndrome, and cancer. Natural killer cells are innate lymphoid cells primarily involved in the immune system response to non-self-components but their plasticity is largely influenced by the pathological microenvironment. Altered NK phenotype and function have been reported in several pathological conditions, basically related to impaired or enhanced toxicity. Here we reviewed and discussed the role of NKs in selected, different, and “distant” chronic diseases, cancer, diabetes, periodontitis, and atherosclerosis, placing NK cells as crucial orchestrator of these pathologic conditions. PMID:28428965

  1. Functional measures, inflammatory markers and endothelin-1 as predictors of 360-day survival in centenarians.

    PubMed

    Szewieczek, Jan; Francuz, Tomasz; Dulawa, Jan; Legierska, Katarzyna; Hornik, Beata; Włodarczyk, Iwona; Janusz-Jenczeń, Magdalena; Batko-Szwaczka, Agnieszka

    2015-10-01

    Centenarians represent a rapidly growing population. To better characterize this specific age group, we have performed a cross-sectional study to observe associations between functional measures and a range of biochemical markers, including inflammatory markers and their significance as predictors of 360-day survival. Medical history and physical and functional assessment (Mini-Mental State Examination (MMSE), Katz Index (activities of daily living, ADL) and Barthel Index (Barthel Index) of Activities of Daily Living, and Lawton Instrumental Activities of Daily Living Scale (Lawton IADL)) were conducted on 86 101.9 ± 1.2-year-old (mean ± SD) subjects (70 women, 16 men). Blood tests were performed on 84 subjects of whom 43 also had extended biomarker assessment. As a reference group 30 51.8 ± 5.0-year old healthy subjects (20 women, 10 men) were recruited. The centenarians received follow-up phone calls. Fifty-two centenarians (60 %) survived ≥360 days. Longer survival was associated with higher MMSE (hazard ratio, HR = 0.934, 95 % confidence interval (CI) 0.896-0.975, P = .002), ADL (HR = 0.840, 95 % CI 0.716-0.985, P = .032), Barthel Index (HR = 0.988, 95 % CI 0.977-0.999, P = .026), and albumin level (HR .926, 95 % CI 0.870-0.986, P .016) and with lower white blood cell (WBC) (HR = 1.161, 95 % CI 1.059-1.273, P = .001), C-reactive protein (CRP) (HR = 1.032, 95 % CI 1.014-1.050, P < .001), IL-6 (HR = 1.182, 95 % CI 1.047-1.335, P = .007), and endothelin-1 (ET-1) level (HR = 3.711, 95 % CI 1.233-11.169, P = .020). Centenarians had higher 360-day survival probability with MMSE ≥13 (P < .001), ADL ≥1 (P < .001), Barthel Index ≥15 (P < .001), Lawton IADL ≥10 points (P = .009), WBC <8.3 G/L (P = .039), CRP <10 mg/L (P < .001), IL-6 <6 pg/mL (P .002), and ET-1 <1.1 pg/mL (P .007). Our results indicate that functional measures, inflammatory markers, and endothelin-1 are predictors of 360-day survival in centenarians.

  2. Effect of periodontal treatment on peak serum levels of inflammatory markers.

    PubMed

    Almaghlouth, Adnan Ali; Cionca, Norbert; Cancela, José Antonio; Décaillet, Fabien; Courvoisier, Delphine S; Giannopoulou, Catherine; Mombelli, Andrea

    2014-12-01

    Some subjects with untreated periodontitis exhibit elevated levels of distinct inflammatory markers in serum. The aim of the study was to assess whether nonsurgical periodontal therapy changes the levels of these markers and lowers these peaks. Forty periodontally diseased subjects received nonsurgical periodontal therapy (full-mouth scaling and root planing within 48 h) with either adjunctive systemic amoxicillin and metronidazole (n = 19) or placebo (n = 21). Serum samples, obtained at baseline (BL) and 3 months after treatment (M3), were evaluated for 15 cytokines and 9 acute-phase proteins using the Bio-Plex bead array multianalyte detection system. For each analyte, peak values were defined as greater than the mean + 2 standard deviations (SD) of measurements found in 40 periodontally healthy persons. Proportions were compared using Fisher's exact test. At M3, a significantly better primary clinical outcome (persisting pockets of >4 mm with bleeding on probing) was obtained in patients treated with scaling and root planing plus antibiotics compared to those receiving placebo (3.3 ± 5.1 vs. 6.8 ± 7.8 pockets per patient, p < 0.05). The levels of cytokines and acute-phase proteins of periodontitis patients were usually below the mean + 2 SD threshold of healthy persons. However, values above threshold were found in some individuals. Eleven patients showed a peak value of one analyte, and seven patients showed two peaks. In the remaining 12 patients, between three and ten analytes showed peak values. Therapy greatly reduced the number of subjects with four or more peaks (BL, 11 subjects; M3, 1 subject, p = 0.003). With regards to the reduction of peaks, no specific benefit of adjunctive antibiotics could be seen. Subjects with untreated periodontitis may show high peaks for several inflammatory markers in serum simultaneously. Nonsurgical periodontal treatment with or without antibiotics reduced most of these peak levels.

  3. Airway Mucin Concentration as a Marker of Chronic Bronchitis.

    PubMed

    Kesimer, Mehmet; Ford, Amina A; Ceppe, Agathe; Radicioni, Giorgia; Cao, Rui; Davis, C William; Doerschuk, Claire M; Alexis, Neil E; Anderson, Wayne H; Henderson, Ashley G; Barr, R Graham; Bleecker, Eugene R; Christenson, Stephanie A; Cooper, Christopher B; Han, MeiLan K; Hansel, Nadia N; Hastie, Annette T; Hoffman, Eric A; Kanner, Richard E; Martinez, Fernando; Paine, Robert; Woodruff, Prescott G; O'Neal, Wanda K; Boucher, Richard C

    2017-09-07

    Chronic obstructive pulmonary disease (COPD) is characterized by chronic bronchitic and emphysematous components. In one biophysical model, the concentration of mucin on the airway surfaces is hypothesized to be a key variable that controls mucus transport in healthy persons versus cessation of transport in persons with muco-obstructive lung diseases. Under this model, it is postulated that a high mucin concentration produces the sputum and disease progression that are characteristic of chronic bronchitis. We characterized the COPD status of 917 participants from the Subpopulations and Intermediate Outcome Measures in COPD Study (SPIROMICS) using questionnaires administered to participants, chest tomography, spirometry, and examination of induced sputum. Total mucin concentrations in sputum were measured with the use of size-exclusion chromatography and refractometry. In 148 of these participants, the respiratory secreted mucins MUC5AC and MUC5B were quantitated by means of mass spectrometry. Data from chronic-bronchitis questionnaires and data on total mucin concentrations in sputum were also analyzed in an independent 94-participant cohort. Mean (±SE) total mucin concentrations were higher in current or former smokers with severe COPD than in controls who had never smoked (3166±402 vs. 1515±152 μg per milliliter) and were higher in participants with two or more respiratory exacerbations per year than in those with zero exacerbations (4194±878 vs. 2458±113 μg per milliliter). The absolute concentrations of MUC5B and MUC5AC in current or former smokers with severe COPD were approximately 3 times as high and 10 times as high, respectively, as in controls who had never smoked. Receiver-operating-characteristic curve analysis of the association between total mucin concentration and a diagnosis of chronic bronchitis yielded areas under the curve of 0.72 (95% confidence interval [CI], 0.65 to 0.79) for the SPIROMICS cohort and 0.82 (95% CI, 0.73 to 0.92) for the

  4. Atherosclerosis: a chronic inflammatory disease mediated by mast cells.

    PubMed

    Conti, Pio; Shaik-Dasthagirisaeb, Yazdami

    2015-01-01

    Inflammation is a process that plays an important role in the initiation and progression of atherosclerosis and immune disease, involving multiple cell types, including macrophages, T-lymphocytes, endothelial cells, smooth muscle cells and mast cells. The fundamental damage of atherosclerosis is the atheromatous or fibro-fatty plaque which is a lesion that causes several diseases. In atherosclerosis the innate immune response, which involves macrophages, is initiated by the arterial endothelial cells which respond to modified lipoproteins and lead to Th1 cell subset activation and generation of inflammatory cytokines and chemoattractant chemokines. Other immune cells, such as CD4+ T inflammatory cells, which play a critical role in the development and progression of atherosclerosis, and regulatory T cells [Treg], which have a protective effect on the development of atherosclerosis are involved. Considerable evidence indicates that mast cells and their products play a key role in inflammation and atherosclerosis. Activated mast cells can have detrimental effects, provoking matrix degradation, apoptosis, and enhancement as well as recruitment of inflammatory cells, which actively contributes to atherosclerosis and plaque formation. Here we discuss the relationship between atherosclerosis, inflammation and mast cells.

  5. [Combination of two signals of danger--a principal cause of activation of chronic inflammatory processes].

    PubMed

    Lebedev, K A

    2012-01-01

    Chronic inflammatory processes have long current during which there is a change of remission by an aggravation of disease. Until recently was considered, that occurrence and activation of chronic inflammatory process is caused by one signal of danger. Most often it are served with microorganisms. The sum of our end literary data shows that activation is connected with accumulation in the center of an inflammation of macrophages and their hyperactivation as a result of action of two signals of danger--microorganisms and xenobiotics.

  6. Inflammatory markers and adipokines alter adipocyte-derived ASP production through direct and indirect immune interaction.

    PubMed

    Lu, H; Gauvreau, D; Tom, F-Q; Lapointe, M; Luo, X P; Cianflone, K

    2013-04-01

    Obesity and related metabolic diseases are associated with chronic low-grade inflammation, characterized by increased pro-inflammatory proteins. Several studies have demonstrated increases in acylation stimulating protein (ASP) and its precursor protein C3 in obesity, diabetes and dyslipidemia. To evaluate the effects of acute inflammatory factors and adipokines on ASP production and potential mechanisms of action, 3T3-L1 adipocytes were treated for 24 h with adipokines, cytokines, macrophage-conditioned media and direct co-culture with J774 macrophages. ASP and C3 in the media were evaluated in relation to changes in adipocyte lipid metabolism (cellular triglyceride stores). Leptin, adiponectin, IL-10, LPS and TNF-α increased ASP production (151%, 153%, 190%, 318%, 134%, P<0.05, respectively,). C5a and RANTES (Regulated and normal T cell expressed and secreted) decreased ASP production ( - 34%, - 47%, P<0.05), which was also associated with a decrease in the precursor protein C3 ( - 39% to - 51%, P<0.01), while keratinocyte chemoattractant (KC; murine IL-8 ortholog) had no effect on ASP and C3 secretion. By contrast, apelin, omentin and visfatin also decreased ASP ( - 27%, - 49%, - 22%, P<0.05), but without changes in precursor protein C3 secretion. Macrophage-conditioned media alone had little effect on C3 or ASP, while co-culture of adipocytes with macrophages markedly increased ASP and C3 production (272%, 167%, P<0.05). These in vitro results suggest various metabolic hormones and inflammatory factors can affect ASP production through increased precursor C3 production and/or by changing the rate of C3 conversion to ASP. As an adipokine, ASP could constitute a new link between adipocytes and macrophages.

  7. Radiation-induced inflammatory markers of brain injury are modulated by PPARdelta activation in vitro and in vivo

    NASA Astrophysics Data System (ADS)

    Schnegg, Caroline Isabel

    As a result of improvements in cancer therapy and health care, the population of long-term cancer survivors is growing. For these approximately 12 million long-term cancer survivors, brain metastases are a significant risk. Fractionated partial or whole-brain irradiation (fWBI) is often required to treat both primary and metastatic brain cancer. Radiation-induced normal tissue injury, including progressive cognitive impairment, however, can significantly affect the well-being of the approximately 200,000 patients who receive these treatments each year. Recent reports indicate that radiation-induced brain injury is associated with chronic inflammatory and oxidative stress responses, as well as increased microglial activation in the brain. Anti-inflammatory drugs may, therefore, be a beneficial therapy to mitigate radiation-induced brain injury. We hypothesized that activation of peroxisomal proliferator activated receptor delta (PPARō) would prevent or ameliorate radiation-induced brain injury, including cognitive impairment, in part, by alleviating inflammatory responses in microglia. For our in vitro studies, we hypothesized that PPARō activation would prevent the radiation-induced inflammatory response in microglia following irradiation. Incubating BV-2 murine microglial cells with the (PPAR)ō agonist, L-165041, prevented the radiation-induced increase in: i) intracellular ROS generation, ii) Cox-2 and MCP-1 expression, and iii) IL-1β and TNF-α message levels. This occured, in part, through PPARō-mediated modulation of stress activated kinases and proinflammatory transcription factors. PPARō inhibited NF-κB via transrepression by physically interacting with the p65 subunit, and prevented activation of the PKCα/MEK1/2/ERK1/2/AP-1 pathway by inhibiting the radiation-induced increase in intracellular ROS generation. These data support the hypothesis that PPARō activation can modulate the radiation-induced oxidative stress and inflammatory

  8. Dysautonomic polyneuropathy as a variant of chronic inflammatory "demyelinating" polyneuropathy?

    PubMed

    Wolf, Hans-Heinrich; Kornhuber, Malte Erich; Weis, Joachim; Posa, Andreas

    2016-08-01

    This report describes the clinical course over almost one decade of a male patient presenting with immune-mediated pure autonomic neuropathy resembling a distinct variant of chronic dysimmune polyneuropathies. We suppose autoantibodies directed against epitopes on autonomic axons or neurons causative for the symptoms.

  9. Ileal inflammatory fibroid polyp causing chronic ileocolic intussusception and mimicking cecal carcinoma

    PubMed Central

    Gara, Naveen; Falzarano, John S; Limm, Whitney ML; Namiki, Thomas S; Tom, Laurie KS

    2009-01-01

    Inflammatory fibroid polyp (IFP) is a rare, idiopathic pseudotumorous lesion of the gastrointestinal tract. While mostly reported as solitary gastric lesions, multiple cases of small bowel IFPs are also reported. It is a documented cause of intussusception in adults. In the case reports of ileal inflammatory fibroid polyps with intussusception, an emergent presentation with small bowel obstruction has been most often described. Here we depict a case of ileal inflammatory fibroid polyp presenting with chronic intermittent ileocolic intussusception, anemia and weight loss with an endoscopic appearance mimicking necrotic cecal carcinoma. PMID:21160780

  10. Acute-onset chronic inflammatory demyelinating polyneuropathy with focal segmental glomerulosclerosis.

    PubMed

    Quek, Amy May Lin; Soon, Derek; Chan, Yee Cheun; Thamboo, Thomas Paulraj; Yuki, Nobuhiro

    2014-06-15

    Inflammatory neuropathies have been reported to occur in association with nephrotic syndrome. Their underlying immuno-pathogenic mechanisms remain unknown. A 50-year-old woman concurrently presented with acute-onset chronic inflammatory demyelinating polyneuropathy and nephrotic syndrome secondary to focal segmental glomerulosclerosis. Both neuropathy and proteinuria improved after plasma exchange and steroids. Literature review of cases of concurrent inflammatory neuropathies and nephrotic syndrome revealed similar neuro-renal presentations. This neuro-renal condition may be mediated by autoantibodies targeting myelin and podocytes.

  11. Iron deficiency across chronic inflammatory conditions: International expert opinion on definition, diagnosis, and management.

    PubMed

    Cappellini, Maria Domenica; Comin-Colet, Josep; de Francisco, Angel; Dignass, Axel; Doehner, Wolfram; S P Lam, Carolyn; Macdougall, Iain C; Rogler, Gerhard; Camaschella, Clara; Kadir, Rezan; Kassebaum, Nicholas J; Spahn, Donat R; Taher, Ali T; Musallam, Khaled M

    2017-10-01

    Iron deficiency, even in the absence of anemia, can be debilitating, and exacerbate any underlying chronic disease, leading to increased morbidity and mortality. Iron deficiency is frequently concomitant with chronic inflammatory disease; however, iron deficiency treatment is often overlooked, partially due to the heterogeneity among clinical practice guidelines. In the absence of consistent guidance across chronic heart failure, chronic kidney disease and inflammatory bowel disease, we provide practical recommendations for iron deficiency to treating physicians: definition, diagnosis, and disease-specific diagnostic algorithms. These recommendations should facilitate appropriate diagnosis and treatment of iron deficiency to improve quality of life and clinical outcomes. © 2017 The Authors American Journal of Hematology Published by Wiley Periodicals, Inc.

  12. Inflammatory markers in gingival crevicular fluid of periodontitis patients with type 2 diabetes mellitus according to glycemic control: A pilot study

    PubMed Central

    Longo, Priscila Larcher; Artese, Hilana Paula Carilo; Horliana, Anna Carolina Ratto Tempestini; Gomes, Giovane Hisse; Romito, Giuseppe Alexandre; Dib, Sergio Atala; Mayer, Marcia Pinto Alves

    2015-01-01

    Background: Type 2 diabetes mellitus (T2DM) and periodontitis are inflammatory conditions with a bidirectional association. This pilot study aimed to evaluate whether T2DM and glycemic control interfere in inflammatory markers profiles in gingival crevicular fluid (GCF) in periodontitis patients. Materials and Methods: Fourteen diabetic periodontitis patients were enrolled in this study, seven with adequate glycemic control (glycated hemoglobin [HbA1c] <8.0%) (DMA + P) and seven with inadequate control (HbA1c ≥8.0%) (DMI + P). Seven chronic periodontitis patients without diabetes formed the control group (P). GCF was obtained from diseased sites (probing depth >6 mm) of an entirely hemiarch, pooled and cytokines levels determined using multiplex beads immunoassay. Clinical periodontal parameters were analyzed by Mann-Whitney test and levels of cytokines by Kruskal-Wallis and Dunn's multiple comparison tests with confidence level of 95% (P < 0.05). Results: Cytokines profile of GCF obtained from deep periodontal pockets presented high levels of inflammatory cytokines, and there were no statistical differences between levels of interleukin-6 (IL-6), IL-8 and tumor necrosis factor-α according to presence of diabetes or percentage of HbA1c among the groups, despite groups with T2DM and periodontitis exhibit higher levels of PD. Conclusion: Within the limitations of this study, inflammatory mediators in GCF are dependent to the local response and do not correlate with the diabetic status. PMID:26604959

  13. Inflammatory markers in gingival crevicular fluid of periodontitis patients with type 2 diabetes mellitus according to glycemic control: A pilot study.

    PubMed

    Longo, Priscila Larcher; Artese, Hilana Paula Carilo; Horliana, Anna Carolina Ratto Tempestini; Gomes, Giovane Hisse; Romito, Giuseppe Alexandre; Dib, Sergio Atala; Mayer, Marcia Pinto Alves

    2015-01-01

    Type 2 diabetes mellitus (T2DM) and periodontitis are inflammatory conditions with a bidirectional association. This pilot study aimed to evaluate whether T2DM and glycemic control interfere in inflammatory markers profiles in gingival crevicular fluid (GCF) in periodontitis patients. Fourteen diabetic periodontitis patients were enrolled in this study, seven with adequate glycemic control (glycated hemoglobin [HbA1c] <8.0%) (DMA + P) and seven with inadequate control (HbA1c ≥8.0%) (DMI + P). Seven chronic periodontitis patients without diabetes formed the control group (P). GCF was obtained from diseased sites (probing depth >6 mm) of an entirely hemiarch, pooled and cytokines levels determined using multiplex beads immunoassay. Clinical periodontal parameters were analyzed by Mann-Whitney test and levels of cytokines by Kruskal-Wallis and Dunn's multiple comparison tests with confidence level of 95% (P < 0.05). Cytokines profile of GCF obtained from deep periodontal pockets presented high levels of inflammatory cytokines, and there were no statistical differences between levels of interleukin-6 (IL-6), IL-8 and tumor necrosis factor-α according to presence of diabetes or percentage of HbA1c among the groups, despite groups with T2DM and periodontitis exhibit higher levels of PD. Within the limitations of this study, inflammatory mediators in GCF are dependent to the local response and do not correlate with the diabetic status.

  14. Perineal Injury During Childbirth Increases Risk of Postpartum Depressive Symptoms and Inflammatory Markers

    PubMed Central

    Dunn, Alexis B.; Paul, Sudeshna; Ware, Laurel Z.; Corwin, Elizabeth J.

    2014-01-01

    Introduction Perineal lacerations during childbirth affect more than 65% of women in the United States. Little attention has been given to the long-term biologic consequences associated with perineal lacerations or possible associations with postpartum mental health. In this article we describe the results of a study that explored inflammatory pathways in women who reported perineal lacerations during childbirth and the relationship with stress and depressive symptoms during the first six months postpartum. Methods A repeated measures design was used to explore the relationship between varying degrees of perineal lacerations, inflammatory cytokines, postpartum stress, and depressive symptoms in 153 women over six months. Depressive symptoms were measured using the Edinburg Postnatal Depression Scale (EPDS) and maternal stress via the Perceived Stress Scale (PSS). Plasma was analyzed for pro (TNF-α, IL-6, IL-1β, IFN-γ) and anti-inflammatory (IL-10) cytokines. Levels of cytokines were compared between women with or without varying degrees of injury. Results A relationship was identified between symptoms of depression and a 2nd degree or more severe perineal laceration starting at 1 month postpartum (P=0.04) and continuing through 3 months (P=0.03). Similarly, stress symptoms were higher at 3 months postpartum (P=0.02). Markers of inflammation were significantly higher among this group with IL-6 increased at 2 weeks postpartum (P=0.02), and remaining elevated through 2 months postpartum (P=0.003); there were also significant differences in pro to anti-inflammatory cytokine ratios out to 6 months postpartum. Regression analysis indicated that 2nd degree or more severe lacerations accounted for 5.9% of the variance in EPDS score at one month postpartum (P=0.024, F=2.865, t=2.127), increasing substantially when the 1-month stress score was included as well. Discussion This study suggests that perineal lacerations, inflammation, stress, and depressed mood are

  15. Chronic administration of methylmalonate on young rats alters neuroinflammatory markers and spatial memory.

    PubMed

    Ribeiro, Leandro Rodrigo; Della-Pace, Iuri Domingues; de Oliveira Ferreira, Ana Paula; Funck, Vinícius Rafael; Pinton, Simone; Bobinski, Franciane; de Oliveira, Clarissa Vasconcelos; da Silva Fiorin, Fernando; Duarte, Marta Maria Medeiros Frescura; Furian, Ana Flávia; Oliveira, Mauro Schneider; Nogueira, Cristina Wayne; Dos Santos, Adair Roberto Soares; Royes, Luiz Fernando Freire; Fighera, Michele Rechia

    2013-09-01

    The methylmalonic acidemia is an inborn error of metabolism (IEM) characterized by methylmalonic acid (MMA) accumulation in body fluids and tissues, causing neurological dysfunction, mitochondrial failure and oxidative stress. Although neurological evidence demonstrate that infection and/or inflammation mediators facilitate metabolic crises in patients, the involvement of neuroinflammatory processes in the neuropathology of this organic acidemia is not yet established. In this experimental study, we used newborn Wistar rats to induce a model of chronic acidemia via subcutaneous injections of methylmalonate (MMA, from 5th to 28th day of life, twice a day, ranged from 0.72 to 1.67 μmol/g as a function of animal age). In the following days (29th-31st) animal behavior was assessed in the object exploration test and elevated plus maze. It was performed differential cell and the number of neutrophils counting and interleukin-1 beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) levels in the blood, as well as levels of IL-1β, TNF-α, inducible nitric oxide synthase (iNOS) and 3-nitrotyrosine (3-NT) in the cerebral cortex were measured. Behavioral tests showed that animals injected chronically with MMA have a reduction in the recognition index (R.I.) when the objects were arranged in a new configuration space, but do not exhibit anxiety-like behaviors. The blood of MMA-treated animals showed a decrease in the number of polymorphonuclear and neutrophils, and an increase in mononuclear and other cell types, as well as an increase of IL-1β and TNF-α levels. Concomitantly, MMA increased levels of IL-1β, TNF-α, and expression of iNOS and 3-NT in the cerebral cortex of rats. The overall results indicate that chronic administration of MMA increased pro-inflammatory markers in the cerebral cortex, reduced immune system defenses in blood, and coincide with the behavioral changes found in young rats. This leads to speculate that, through mechanisms not yet elucidated, the

  16. Clinical and electrophysiological parameters distinguishing acute-onset chronic inflammatory demyelinating polyneuropathy from acute inflammatory demyelinating polyneuropathy.

    PubMed

    Dionne, Annie; Nicolle, Michael W; Hahn, Angelika F

    2010-02-01

    Up to 16% of chronic inflammatory demyelinating polyneuropathy (CIDP) patients may present acutely. We performed a retrospective chart review on 30 acute inflammatory demyelinating polyneuropathy (AIDP) and 15 acute-onset CIDP (A-CIDP) patients looking for any clinical or electrophysiological parameters that might differentiate AIDP from acutely presenting CIDP. A-CIDP patients were significantly more likely to have prominent sensory signs. They were significantly less likely to have autonomic nervous system involvement, facial weakness, a preceding infectious illness, or need for mechanical ventilation. With regard to electrophysiological features, neither sural-sparing pattern, sensory ratio >1, nor the presence of A-waves was different between the two groups. This study suggests that patients presenting acutely with a demyelinating polyneuropathy and the aforementioned clinical features should be closely monitored as they may be more likely to have CIDP at follow-up.

  17. Blood dendritic cells: “canary in the coal mine” to predict chronic inflammatory disease?

    PubMed Central

    Miles, Brodie; Abdel-Ghaffar, Khaled A.; Gamal, Ahmed Y.; Baban, Babak; Cutler, Christopher W.

    2014-01-01

    The majority of risk factors for chronic inflammatory diseases are unknown. This makes personalized medicine for assessment, prognosis, and choice of therapy very difficult. It is becoming increasingly clear, however, that low-grade subclinical infections may be an underlying cause of many chronic inflammatory diseases and thus may contribute to secondary outcomes (e.g., cancer). Many diseases are now categorized as inflammatory-mediated diseases that stem from a dysregulation in host immunity. There is a growing need to study the links between low-grade infections, the immune responses they elicit, and how this impacts overall health. One such link explored in detail here is the extreme sensitivity of myeloid dendritic cells (mDCs) in peripheral blood to chronic low-grade infections and the role that these mDCs play in arbitrating the resulting immune responses. We find that emerging evidence supports a role for pathogen-induced mDCs in chronic inflammation leading to increased risk of secondary clinical disease. The mDCs that are elevated in the blood as a result of low-grade bacteremia often do not trigger a productive immune response, but can disseminate the pathogen throughout the host. This aberrant trafficking of mDCs can accelerate systemic inflammatory disease progression. Conversely, restoration of dendritic cell homeostasis may aid in pathogen elimination and minimize dissemination. Thus it would seem prudent when assessing chronic inflammatory disease risk to consider blood mDC numbers, and the microbial content (microbiome) and activation state of these mDCs. These may provide important clues (“the canary in the coal mine”) of high inflammatory disease risk. This will facilitate development of novel immunotherapies to eliminate such smoldering infections in atherosclerosis, cancer, rheumatoid arthritis, and pre-eclampsia. PMID:24478766

  18. [Autoantibodies in children with chronic inflammatory lung diseases].

    PubMed

    Markina, O A; Iastrebova, N E; Vaneeva, N P; Volkov, I K; Katosova, L K

    2001-01-01

    124 sera of children with chronic bronchitis, chronic pneumonia, bronchial asthma, exogenic allergic alveolitis, congenital developmental defects of the lungs and the syndrome of the situs inversus of organs were examined with a view to study the state of humoral immunity to tissues. The study was carried out by means of the enzyme-linked immunosorbent assay with the use of collagen, elastin, DNA (native and denaturated), membrane antigens of the lung, the liver, the small intestine and the large intestine. Among all groups of patients autoimmune disturbances, manifested by a rise in the level of autoantibodies of different specificity, were registered. The degree of manifestation of autoimmune disturbances depended on the kind of pathology. After treatment a decrease in the level of autoantibodies was registered in the examinees.

  19. Anti-steatotic and anti-inflammatory effects of Hovenia dulcis Thunb. extracts in chronic alcohol-fed rats.

    PubMed

    Choi, Ra-Yeong; Woo, Moon-Jae; Ham, Ju Ri; Lee, Mi-Kyung

    2017-04-02

    The anti-steatotic and anti-inflammatory effects of fruit water extract (FW) and seed ethanol extract (SE) of Hovenia dulcis Thunb. in chronic alcohol-fed rats were investigated. Rats were fed a liquid diet containing 36% calories from alcohol and orally administered FW or SE (300 and 500mg/kg/day). Both FW and SE reduced hepatic lipid contents and droplets, serum lipid concentration and inflammatory markers (hs-CRP, TNF-α and IL-6) levels compared with the alcohol control group. Alcohol led to significant decreases in the hepatic fatty acid oxidative gene (Ppargc1a, Cpt1a and Acsl1) levels, while it significantly increased the Myd88 and Tnfa gene levels. However, FW or SE supplementation significantly up-regulated gene expression of Ppargc1a, Ppara, Cpt1a and Acsl1, and down-regulated gene expression of Myd88, Tnfa and Crp compared with the alcohol control group. FW or SE supplementation also significantly decreased hepatic activities of fatty acid synthase and phosphatidate phosphohydrolase in chronic alcohol-fed rats. Plasma alcohol and acetaldehyde levels, hepatic enzyme activity and protein expression of CYP2E1 were lowered by FW or SE supplementation. These results indicate that both FW and SE play an important role in improvement of alcoholic hepatic steatosis and inflammation via regulation of lipid and inflammation metabolism.

  20. Negative-pressure Wound Therapy in Chronic Inflammatory Breast Diseases

    PubMed Central

    Namdaroğlu, Ozan Barış; Yazıcı, Hilmi; Öztürk, Ahmet Mücteba; Yakan, Savaş; Yıldırım, Mehmet; Uçar, Ahmet Deniz; Erkan, Nazif

    2016-01-01

    Mastitis is inflammation of breast tissue that may or may not originate from an infection. Two different forms of mastitis have been described, lactational and non-lactational. Lactational mastitis is the most common type and generally conservative therapy that includes milk removal and physical therapy provides symptomatic relief, but antibiotic therapy is also needed. Common types of non-lactational mastitis are periductal mastitis and idiopathic granulomatous mastitis. Treatment includes antibiotics, drainage, and surgery, but usually this is a chronic process and a therapeutic management algorithm for chronic breast inflammation is unclear and has no consensus. Negative-pressure wound therapy is commonly used for various types of wounds but is limited for breast wounds. In this report, we present and discuss two patients with chronic breast inflammation who underwent surgery and were successfully treated using negative-pressure wound therapy to minimize wide tissue defects and cosmetic problems after surgery. Use of negative-pressure wound therapy for breast wounds might be benefical as it is with other wounds but there is scarce information in the literature

  1. Do inflammatory markers portend heterotopic ossification and wound failure in combat wounds?

    PubMed

    Forsberg, Jonathan A; Potter, Benjamin K; Polfer, Elizabeth M; Safford, Shawn D; Elster, Eric A

    2014-09-01

    After a decade of war in Iraq and Afghanistan, we have observed an increase in combat-related injury survival and a paradoxical increase in injury severity, mainly because of the effects of blasts. These severe injuries have a devastating effect on each patient's immune system resulting in massive upregulation of the systemic inflammatory response. By examining inflammatory mediators, preliminary data suggest that it may be possible to correlate complications such as wound failure and heterotopic ossification (HO) with distinct systemic and local inflammatory profiles, but this is a relatively new topic. We asked whether systemic or local markers of inflammation could be used as an objective means, independent of demographic and subjective factors, to estimate the likelihood of (1) HO and/or (2) wound failure (defined as wounds requiring surgical débridement after definitive closure, or wounds that were not closed or covered within 21 days of injury) in patients sustaining combat wounds. Two hundred combat wounded active-duty service members who sustained high-energy extremity injuries were prospectively enrolled between 2008 and 2012. Of these 200 patients, 189 had adequate followups to determine the presence or absence of HO, and 191 had adequate followups to determine the presence or absence of wound failure. In addition to injury-specific and demographic data, we quantified 24 cytokines and chemokines during each débridement. Patients were followed clinically for 6 weeks, and radiographs were obtained 3 months after definitive wound closure. Associations were investigated between these markers and wound failure or HO, while controlling for known confounders. The presence of an amputation (p < 0.001; odds ratio [OR], 6.1; 95% CI. 1.63-27.2), Injury Severity Score (p = 0.002; OR, 33.2; 95% CI, 4.2-413), wound surface area (p = 0.001; OR, 1.01; 95% CI, 1.002-1.009), serum interleukin (IL)-3 (p = 0.002; OR, 2.41; 95% CI, 1.5-4.5), serum IL-12p70 (p = 0.01; OR, 0

  2. Influences of the common FTO rs9939609 variant on inflammatory markers throughout a broad range of body mass index.

    PubMed

    Zimmermann, Esther; Skogstrand, Kristin; Hougaard, David M; Astrup, Arne; Hansen, Torben; Pedersen, Oluf; Sørensen, Thorkild I A; Jess, Tine

    2011-01-05

    A recent study reported that the fatness associated A-allele of FTO rs9939609 increased plasma high sensitivity C-reactive protein (hs-CRP) levels independent of fatness. We aimed to investigate if this gene variant had fatness-independent effects on plasma hs-CRP and 10 additional circulating obesity-related adipokines throughout a broad range of body mass index (BMI) among Danish men. In a population of 362,200 young men, examined for military service between 1943 and 1977, two groups were identified: 1) a random 1% sample and 2) all obese men (BMI = 31.0 kg/m(2), all of whom were above the 99(th) percentile of this population). At an average age of 49 years (range: 39 through 65 years), 551 men, hereof 231 of the obese, were re-examined, including genotyping and measurement of the fasting circulating inflammatory markers hs-CRP, IL-1β, IL-6, IL-10, IL-18, mip1α, mip1β, sTNFα-R1, TGF-β, TNF-α and leptin. Men with known disease were excluded from the examination. All the inflammatory markers were log-transformed to approximate a normal distribution. Genotype-phenotype relationships were studied using linear regression analyses with the inflammatory markers as the response variable. Significant positive associations between hs-CRP, leptin and a broad range of BMI were observed, but the associations did not significantly differ across FTO rs9939609 genotype. There were no significant associations between the other inflammatory markers, FTO rs9939609 genotype or BMI, respectively. No fatness-independent effects of the FTO rs9939609 A-allele on a series of inflammatory markers were observed in this cohort of healthy middle-aged men representing a broad range of fatness.

  3. Influences of the Common FTO rs9939609 Variant on Inflammatory Markers Throughout a Broad Range of Body Mass Index

    PubMed Central

    Zimmermann, Esther; Skogstrand, Kristin; Hougaard, David M.; Astrup, Arne; Hansen, Torben; Pedersen, Oluf; Sørensen, Thorkild I. A.; Jess, Tine

    2011-01-01

    Background A recent study reported that the fatness associated A-allele of FTO rs9939609 increased plasma high sensitivity C-reactive protein (hs-CRP) levels independent of fatness. We aimed to investigate if this gene variant had fatness-independent effects on plasma hs-CRP and 10 additional circulating obesity-related adipokines throughout a broad range of body mass index (BMI) among Danish men. Methodology/Principal Findings In a population of 362,200 young men, examined for military service between 1943 and 1977, two groups were identified: 1) a random 1% sample and 2) all obese men (BMI = 31.0 kg/m2, all of whom were above the 99th percentile of this population). At an average age of 49 years (range: 39 through 65 years), 551 men, hereof 231 of the obese, were re-examined, including genotyping and measurement of the fasting circulating inflammatory markers hs-CRP, IL-1β, IL-6, IL-10, IL-18, mip1α, mip1β, sTNFα-R1, TGF-β, TNF-α and leptin. Men with known disease were excluded from the examination. All the inflammatory markers were log-transformed to approximate a normal distribution. Genotype-phenotype relationships were studied using linear regression analyses with the inflammatory markers as the response variable. Significant positive associations between hs-CRP, leptin and a broad range of BMI were observed, but the associations did not significantly differ across FTO rs9939609 genotype. There were no significant associations between the other inflammatory markers, FTO rs9939609 genotype or BMI, respectively. Conclusion No fatness-independent effects of the FTO rs9939609 A-allele on a series of inflammatory markers were observed in this cohort of healthy middle-aged men representing a broad range of fatness. PMID:21246032

  4. The occurrence of preterm delivery is linked to pregnancy-specific distress and elevated inflammatory markers across gestation.

    PubMed

    Coussons-Read, Mary E; Lobel, Marci; Carey, J Chris; Kreither, Marianne O; D'Anna, Kimberly; Argys, Laura; Ross, Randall G; Brandt, Chandra; Cole, Stephanie

    2012-05-01

    There is mounting evidence that stress during pregnancy can have detrimental effects on gestation and birth. Existing studies indicate that prenatal stress may increase levels of circulating inflammatory markers that are associated with prematurity and pregnancy complications, suggesting that stress-related changes in the cytokine milieu may increase the risk of poor pregnancy outcome. Previous studies, however, have not clearly connected stress during pregnancy to changes in inflammatory mediators and, in turn, to clinically-relevant outcomes such as premature delivery. The present study sought to directly connect prenatal stress and changes in inflammatory markers to preterm delivery and gestational age at birth (GAB). A sample of 173 women was recruited during the first trimester of pregnancy and followed through delivery. Overall stress, pregnancy-specific distress, and inflammatory markers were assessed early and later in pregnancy, and the predictive value of these measures for preterm birth and GAB was determined. There were significant differences in pregnancy-specific distress, IL-6, and TNF-α between women who delivered prematurely versus those who delivered at term, and elevated levels of pregnancy-specific distress, IL-6, and TNF-α were predictive of shortened GAB overall. Importantly, in many cases, the effects of overall stress and pregnancy-specific distress on GAB were mediated by levels of circulating inflammatory markers. Collectively, these data provide strong evidence that prenatal stress experiences can affect the timing of parturition via alterations in circulating inflammatory mediators, and underscore the need for ongoing research aimed at further understanding the mechanisms and effects of prenatal stress on maternal and infant health. Copyright © 2012 Elsevier Inc. All rights reserved.

  5. NTPDase and 5'-nucleotidase as inflammatory markers in cattle naturally infected by Eurytrema coelomaticum.

    PubMed

    Fávero, Juscivete F; Schwertz, Claiton I; Doleski, Pedro H; Leal, Daniela B R; Machado, Gustavo; Manzoni, Alessandra G; da Silva, Ester S; Gabriel, Mateus E; Stedille, Fernanda A; Christ, Ricardo; Stefani, Lenita M; Mendes, Ricardo E; da Silva, Aleksandro S

    2016-10-01

    The aim of this study was to evaluate seric NTPDase and 5'nucleotidase activities of cattle naturally infected by Eurytrema coelomanticum, as well as to correlate them to histopathological lesions in the pancreas and the degree of parasitism. Blood samples and pancreas of 51 bovines were collected on a slaughterhouse in Southern Brazil: 33 from cattle naturally infected by E. coelomanticum (the Group A), and 18 from uninfected animals (the Group B). Infected animals showed an average of 532 parasites per pancreas. In the pancreatic histology, ducts displayed hyperplasia, stenosis, proliferation of fibrous tissue, and interstitial inflammatory infiltration of lymphocytes. The serum from infected animals showed an increase in NTPDase activity when ATP was used as substrate (P<0.001). For the ADP substrate, there was no difference between groups regarding NTPDase activity (P=0.37), as well as 5'-nucleotidase activity (P=0.27). Correlating NTPDase activity (ATP substrate) with the degree of histopathological lesions (rho=0.66, P<0.001) and the parasitic load on the pancreas (rho=0.65, P<0.001), a positive correlation was observed. Similar results were found between the degree of histopathological lesions and NTPDase activity (ADP substrate; rho=0.29, P=0.03), and 5'nucleotidase activity (rho=0.35, P=0.01). Based on the results of NTPDase and 5'nucleotidase enzymes in cattle naturally infected by E. coleomanticum, it is possible to suggest that these enzymes are involved in the modulation of inflammation, and they can act as markers of inflammatory response. Copyright © 2016 Elsevier Ltd. All rights reserved.

  6. Inflammatory transcription factors as activation markers and functional readouts in immune-to-brain communication.

    PubMed

    Rummel, Christoph

    2016-05-01

    Immune-to-brain communication pathways involve humoral mediators, including cytokines, central modulation by neuronal afferents and immune cell trafficking to the brain. During systemic inflammation these pathways contribute to mediating brain-controlled sickness symptoms including fever. Experimentally, activation of these signaling pathways can be mimicked and studied when injecting animals with pathogen associated molecular patterns (PAMPS). One central component of the brain inflammatory response, which leads, for example, to fever induction, is transcriptional activation of brain cells via cytokines and PAMPS. We and others have studied the spatiotemporal activation and the physiological significance of transcription factors for the induction of inflammation within the brain and the manifestation of fever. Evidence has revealed a role of nuclear factor (NF)κB in the initiation, signal transducer and activator of transcription (STAT)3 in the maintenance and NF-interleukin (IL)6 in the maintenance or even termination of brain-inflammation and fever. Moreover, psychological stressors, such as exposure to a novel environment, leads to increased body core temperature and genomic NF-IL6-activation, suggesting a potential use of NF-IL6-immunohistochemistry as a multimodal brain cell activation marker and a role for NF-IL6 for differential brain activity. In addition, the nutritional status, as reflected by circulating levels of the cytokine-like hormone leptin, influence immune-to-brain communication and age-dependent changes in LPS-induced fever. Overall, transcription factors remain therapeutically important targets for the treatment of brain-inflammation and fever induction during infectious/non-infectious inflammatory and psychological stress. However, the exact physiological role and significance of these transcription factors requires to be further investigated.

  7. Analysis of inflammatory markers and metals in nasal lavage fluid of welders.

    PubMed

    Raulf, Monika; Weiss, Tobias; Lotz, Anne; Lehnert, Martin; Hoffmeyer, Frank; Liebers, Verena; Van Gelder, Rainer; Udo Käfferlein, Heiko; Hartwig, Andrea; Pesch, Beate; Brüning, Thomas

    2016-01-01

    Welding fumes may produce adverse health effects in the respiratory tract. To assess the relationship between exposure to welding fumes and inflammation in the upper airways, 190 male welders were examined from the WELDOX study (median age 40 yr, 54.7% smokers, and 32.9% atopics). Inhalable welding fumes were collected in the breathing zone of welders during a single shift. Chromium (Cr), nickel (Ni), manganese (Mn), and iron (Fe) were measured in the welding-fume samples and in postshift nasal lavage fluid (NALF). In addition, the numbers of particles and inflammatory biomarkers, including total and differential cell counts, interleukin (IL)-8, leukotriene (LT) B4, 8-isoprostane (8-iso-PGF2α), tissue inhibitor of metalloproteinase-1 (TIMP-1), and immunoreactive matrix metalloproteinase (MMP)-9, were determined. Metal concentrations in NALF correlated with airborne concentrations. No significant association was found between airborne metal concentrations and biomarkers of inflammation in NALF, whereas increasing metal concentrations in NALF resulted in increased concentrations of total protein, IL-8, MMP-9, and TIMP-1. LTB4 and 8-iso PGF2α were elevated at higher concentrations of Cr or Ni in NALF. The same was true for Fe, although the effects were less pronounced and of borderline significance. In conclusion, our results showed a significant association between the concentrations of metals and soluble inflammatory markers in the NALF of welders. The noninvasive collection of NALF is applicable in field studies, where it may serve as a suitable matrix to simultaneously assess biomarkers of exposure and effect in the upper respiratory tract in workers who are occupationally exposed to airborne hazardous substances.

  8. Serum levels of neopterin, inflammatory markers and oxidative stress indicators in hyperemesis gravidarum.

    PubMed

    Tunc, Senem Yaman; Agacayak, Elif; Budak, Sukru; Tunc, Nurettin; Icen, Mehmet Sait; Findik, Fatih Mehmet; Ekinci, Aysun; Gul, Talip

    2016-06-01

    To investigate whether serum levels of neopterin and inflammatory markers including C-reactive protein (CRP), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and oxidative status indicators were altered in patients with hyperemesis gravidarum (HG) compared to asymptomatic pregnant women. This cross-sectional study was performed including 30 pregnant women with HG (mean age: 30.67 ± 6.68) and 30 asymptomatic pregnant women (mean age: 28.00 ± 5.30). Demographic features, obstetric history, and the Pregnancy Unique Quantification of Emesis/Nausea (PUQE) index were noted. Complete blood count, serum biochemical assay and measurement of CRP, TNF-α, IL-6, total antioxidant status and total oxidative status (TOS) levels were taken and compared between groups. White blood cell count (P = 0.013), platelet count (P = 0.015), TOS (P < 0.001), and PUQE score (P < 0.001) were remarkably higher in HG pregnancies. On the other hand, serum levels of lactate dehydrogenase, (P < 0.001), sodium (P < 0.001), potassium (P < 0.001), chloride (P < 0.001) and TAS (P < 0.001) were higher in the control group. There was no difference in the levels of neopterin, CRP, TNF-α and IL-6. In patients with HG, a positive correlation was detected between TOS and serum levels of lactate dehydrogenase, while TNF-α, IL-6 and neopterin were positively correlated with hemoglobin levels. Our results demonstrated no association between inflammation and HG. Elucidation of the pathophysiology and complex interaction between various inflammatory processes in HG necessitates further trials on larger series. © 2016 Japan Society of Obstetrics and Gynecology.

  9. Interaction of Vitamin D and Smoking on Inflammatory Markers in the Urban Elderly

    PubMed Central

    Lee, Hyemi; Kim, Kyoung-Nam; Lim, Youn-Hee; Hong, Yun-Chul

    2015-01-01

    Objectives: Epidemiological studies have reported that vitamin D deficiency is associated with inflammatory disease. Smoking is a well-known risk factor for inflammation. However, few studies have investigated the interactive effect of vitamin D deficiency and smoking on inflammation. This study aims to investigate the interaction of vitamin D and smoking with inflammatory markers in the urban elderly. Methods: We used data from the Korean Elderly Environmental Panel Study, which began in August 2008 and ended in August 2010, and included 560 Koreans ≥60 years old living in Seoul. Data was collected via questionnaires that included items about smoking status at the first visit. Vitamin D levels, high-sensitivity C-reactive protein (hs-CRP), and white blood cell (WBC) counts were repeatedly measured up to three times. Results: The association of vitamin D and hs-CRP was significant after adjusting for known confounders (β=-0.080, p=0.041). After separate analysis by smoking status, the association of vitamin D deficiency and hs-CRP in smokers was stronger than that in nonsmokers (smokers: β=-0.375, p=0.013; non-smokers: β=-0.060, p=0.150). Smoking status was an effect modifier that changed the association between vitamin D deficiency and hs-CRP (interaction estimate: β=-0.254, p=0.032). Vitamin D was not significantly associated with WBC count (β=0.003, p=0.805). Conclusions: Vitamin D deficiency was associated with hs-CRP in the urban elderly. Smoking status was an effect modifier of this association. Vitamin D deficiency was not significantly associated with WBC count. PMID:26429291

  10. Association between Inflammatory Marker, Environmental Lead Exposure, and Glutathione S-Transferase Gene

    PubMed Central

    Sirivarasai, Jintana; Wananukul, Winai; Kaojarern, Sming; Chanprasertyothin, Suwannee; Thongmung, Nisakron; Ratanachaiwong, Wipa; Sura, Thanyachai; Sritara, Piyamit

    2013-01-01

    A number of studies suggested that lead is related to the induction of oxidative stress, and alteration of immune response. In addition, modifying these toxic effects varied partly by GST polymorphism. The objectives of this study were to assess the association between the lead-induced alteration in serum hs-CRP, with GSTM1, GSTT1, and GSTP1 Val105Ile genetic variations and the health consequence from environmental lead exposure. The 924 blood samples were analyzed for blood lead, CRP, and genotyping of three genes with real-time PCR. Means of blood lead and serum hs-CRP were 5.45 μg/dL and 2.07 mg/L. Both CRP and systolic blood pressure levels were significantly higher for individuals with blood lead in quartile 4 (6.48–24.63 μg/dL) compared with those in quartile 1 (1.23–3.47 μg/dL, P < 0.01). In particular, in men with blood lead >6.47 μg/dL the adjusted odds ratio (OR) of CRP levels for individuals with GSTP1 variants allele, GSTM1 null, GSTT1 null, double-null GSTM1, and GSTT1 compared with wild-type allele was 1.46 (95% CI; 1.05–2.20), 1.32 (95% CI; 1.03–1.69), 1.65 (95% CI; 1.17–2.35), and 1.98 (95% CI; 1.47–2.55), respectively. Our findings suggested that lead exposure is associated with adverse changes in inflammatory marker and SBP. GST polymorphisms are among the genetic determinants related to lead-induced inflammatory response. PMID:23484121

  11. Herpesviruses, Inflammatory Markers and Incident Depression in a Longitudinal Study of Detroit Residents

    PubMed Central

    Simanek, Amanda M.; Cheng, Caroline; Yolken, Robert; Uddin, Monica; Galea, Sandro; Aiello, Allison E.

    2014-01-01

    Background Depression is predicted to become the leading cause of disability worldwide by 2030 and moreover, socioeconomic inequalities in depression persist. Herpesviruses, which are more prevalent among socioeconomically disadvantaged populations, subject to stress-induced reactivation and are associated with increased levels of pro-inflammatory cytokines implicated in the etiology of depression, may serve as novel risk factors for depression onset. Methods Data are from individuals in the Detroit Neighborhood Health Study tested for herpes simplex virus-1 (HSV-1) and cytomegalovirus (CMV) seropositivity/Immunoglobulin G (IgG) antibody levels (N=263) as well as interleukin-6 (IL-6) (N=245) and C-reactive protein (CRP) (N=236) levels and assessed for incident depression via the Patient Health Questionnaire-9. Linear and logistic regression models were used to examine associations between pathogen seropositivity/IgG antibody levels, pro-inflammatory markers and incident depression over approximately one-year of follow-up. Results For every one unit increase in CMV IgG antibody level, the odds of incident depression increased by 26% and individuals with IgG antibody levels in the highest quartile had over three times greater odds of incident depression (odds ratio 3.87, 95% confidence interval 1.47, 10.19), compared to those in the lower three quartiles. Neither CMV or HSV-1 seropositivity nor HSV-1 IgG antibody level were associated with IL-6 or CRP levels at Wave 1, nor were IL-6 or CRP levels associated with incident depression at Wave 2. Conclusions Further examination of the biological pathways linking CMV and depression are warranted. PMID:25218654

  12. Acute effects of different alcoholic beverages on vascular endothelium, inflammatory markers and thrombosis fibrinolysis system.

    PubMed

    Tousoulis, Dimitris; Ntarladimas, Ioannis; Antoniades, Charalambos; Vasiliadou, Carmen; Tentolouris, Costas; Papageorgiou, Nikos; Latsios, George; Stefanadis, Christodoulos

    2008-08-01

    Mild alcohol consumption has been associated with decreased cardiovascular risk, although the underlying mechanisms are still unclear. We compared the acute effects of several alcoholic beverages on endothelial function, inflammatory process and thrombosis/fibrinolysis system in young adults. In this randomized intervention trial, healthy young individuals with no risk factor for atherosclerosis were randomized into 5 equally sized groups and received an equal amount of alcohol (30 g), as red wine (264 ml), white wine (264 ml), beer (633 ml), whisky (79 ml) or water (250 ml). Forearm blood flow was determined by gauge-strain plethysmography, at baseline, 1 and 4 h after alcohol intake. Levels of interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-alpha), C-reactive protein (CRP), fibrinogen (Fib), plasminogen activator inhibitor (PAI-1), von Willebrand factor (vWF) and tissue plasminogen activator (tPA) were determined at baseline and 4 h after alcohol consumption. Reactive hyperemia was significantly increased 1 h after beer and red wine consumption (p<0.05 for both), while it returned at baseline at 4 h (p=ns vs baseline) but remained unchanged in all the other groups. vWF was decreased in the beer and red wine groups (p<0.05 for both) only. PAI-1/tPA ratio remained unchanged only in red wine and control group. Inflammatory markers remained unchanged in all the groups. Acute consumption of red wine or beer improves endothelial function and decreases vWF levels, suggesting that the type of beverage may differently affect endothelial function and thrombosis/fibrinolysis system in healthy adults.

  13. Carbocysteine: clinical experience and new perspectives in the treatment of chronic inflammatory diseases.

    PubMed

    Macciò, Antonio; Madeddu, Clelia; Panzone, Filomena; Mantovani, Giovanni

    2009-03-01

    Carbocysteine is a muco-active drug with free radical scavenging and anti-inflammatory properties. It is actually approved for clinical use as adjunctive therapy of respiratory tract disorders characterized by excessive, viscous mucus, including chronic obstructive airways disease (COPD). The intriguing antioxidant and anti-inflammatory properties of carbocysteine, beyond its known mucolytic activity, are described to explain its therapeutic efficacy and suggest new clinical uses. After reviewing physiology and preclinical studies, human studies on the use of carbocysteine in chronic inflammatory diseases, i.e., COPD and cancer cachexia, are reviewed. Carbocysteine has been recently recognized as an effective and safe treatment for the long-term management of COPD, able to reduce the incidence of exacerbations and improve patient quality of life. Moreover, carbocysteine was effective in counteracting some symptoms associated with cancer cachexia. Preclinical and clinical studies have demonstrated that the antioxidant and anti-inflammatory properties of carbocysteine are more important than mucolysis itself for its therapeutic efficacy. Therefore, carbocysteine may be able to reverse the oxidative stress associated with several chronic inflammatory diseases, such as cardiovascular diseases and neurodegenerative disorders. Controlled, randomized studies in humans are warranted.

  14. Adiponectin: an attractive marker for metabolic disorders in Chronic Obstructive Pulmonary Disease (COPD).

    PubMed

    Bianco, Andrea; Mazzarella, Gennaro; Turchiarelli, Viviana; Nigro, Ersilia; Corbi, Graziamaria; Scudiero, Olga; Sofia, Matteo; Daniele, Aurora

    2013-10-14

    Chronic Obstructive Pulmonary Disease (COPD) is a chronic inflammatory lung disease which may be complicated by development of co-morbidities including metabolic disorders. Metabolic disorders commonly associated with this disease contribute to lung function impairment and mortality. Systemic inflammation appears to be a major factor linking COPD to metabolic alterations. Adipose tissue seems to interfere with systemic inflammation in COPD patients by producing a large number of proteins, known as "adipokines", involved in various processes such as metabolism, immunity and inflammation. There is evidence that adiponectin is an important modulator of inflammatory processes implicated in airway pathophysiology. Increased serum levels of adiponectin and expression of its receptors on lung tissues of COPD patients have recently highlighted the importance of the adiponectin pathway in this disease. Further, in vitro studies have demonstrated an anti-inflammatory activity for this adipokine at the level of lung epithelium. This review focuses on mechanisms by which adiponectin is implicated in linking COPD with metabolic disorders.

  15. Faecal calprotectin, an useful marker in discriminating between inflammatory bowel disease and functional gastrointestinal disorders.

    PubMed

    Lozoya Angulo, Maria Elena; de Las Heras Gómez, Ignacio; Martinez Villanueva, Miriam; Noguera Velasco, Jose Antonio; Avilés Plaza, Francisco

    2017-03-01

    Diagnostic discrimination between inflammatory bowel disease (IBD) and functional gastrointestinal disorders is complex, as they cause similar signs and symptoms. Faecal calprotectin (FC) is a useful marker in this context, and can be used to select patients who will most benefit from colonoscopy. The aim of this study was to evaluate the utility of FC in discriminating between organic disease and functional disorders. The study included 264 patients presenting with gastrointestinal complaints consistent with an organic pathology. FC levels were determined and diagnostic accuracy was assessed using the area under the curve obtained from the final diagnosis. Calprotectin levels in organic bowel disease patients were significantly higher (median 254μg/g; 95% confidence interval [CI], interquartile range 105-588.5) than in functional disease patients (95μg/g; 95% CI, 47.25-243.92) (P<.0001). Similarly, in patients with IBD, the values obtained were higher (270.85μg/g; 95% CI, 96.85-674.00) than in those with irritable bowel syndrome (79.70μg/g; 95% CI, 36.50-117.25) (P<.0001). For a cut-off of 150μg/g, FC had an area under the ROC curve to discriminate between organic and functional disease of 0.718, and 0.872 to discriminate between irritable bowel syndrome and IBD. Our study supports the importance of FC as a marker in the evaluation of patients with IBD. The best diagnostic accuracy is obtained at a cut-off value of 150μg/g. Copyright © 2016 Elsevier España, S.L.U., AEEH y AEG. All rights reserved.

  16. Traffic-related air pollution affects peak expiratory flow, exhaled nitric oxide, and inflammatory nasal markers.

    PubMed

    Steerenberg, P A; Nierkens, S; Fischer, P H; van Loveren, H; Opperhuizen, A; Vos, J G; van Amsterdam, J G

    2001-01-01

    The authors used a longitudinal observational design, with repeated measures, to study the association between traffic-related air pollutants (i.e., nitric oxide, nitrogen dioxide, carbon monoxide, and Black Smoke) and respiratory symptoms. Subjects (N = 82) attended an elementary school in either Utrecht (i.e., urban children) or Bilthoven (i.e., suburban children). These two geographic areas differed with respect to levels of Black Smoke (means = 53 microg/m3 and 18 microg/m3, respectively). Levels of nitric oxide, nitrogen dioxide, carbon monoxide, and Black Smoke were consistently higher in Utrecht than in Bilthoven (mean daily ratios were 8, 1.5, 1.8, and 2.7, respectively). The authors compared mean levels of short-term effects of the aforementioned air pollutants on suburban and urban children. Urban children had higher mean levels (p = .05) of interleukin-8 (32%), urea (39%), uric acid (26%), albumin (15%), and nitric oxide metabolites (21%) in nasal lavage than did suburban children. Peak expiratory flow, exhaled nitric oxide levels, and nasal markers were associated with levels of particulate matter with diameters less than or equal to 10 microm, Black Smoke, nitrogen dioxide, and nitric oxide. With respect to per-unit increases in air pollution, urban children had more increased peak expiratory flow, higher levels of exhaled nitric oxide, and more increased release of uric acid, urea, and nitric oxide metabolites than suburban children. In summary, urban children had increased levels of inflammatory nasal markers, and their responses were more pronounced than were the suburban children's responses to the same increments of air pollution.

  17. Inflammatory markers, rather than conventional risk factors, are different between carotid and MCA atherosclerosis

    PubMed Central

    Bang, O; Lee, P; Yoon, S; Lee, M; Joo, I; Huh, K

    2005-01-01

    Background: The apparent differences in risk factors for intra- and extracranial atherosclerosis are unclear and the mechanisms that underlie strokes in patients with intracranial atherosclerosis are not well known. We investigated the conventional vascular risk factors as well as other factors in stroke patients with large artery atherosclerosis. Methods: Using diffusion weighted imaging (DWI) and vascular and cardiologic studies, we selected patients with acute non-cardioembolic cerebral infarcts within the middle cerebral artery (MCA) territory. Patients were divided into two groups: those with atherosclerotic lesions on the carotid sinus (n = 112) and those with isolated lesions on the proximal MCA (n = 160). Clinical features, risk factors, and DWI patterns were compared between groups. Results: There were no differences in conventional risk factors, but markers for inflammation were significantly higher in patients with carotid atherosclerosis than in those with isolated MCA atherosclerosis (p<0.01 for both). After adjustments for age/sex and the severity of stroke, an inverse correlation was observed between C-reactive protein levels and MCA atherosclerosis (odds ratio 0.57 per 1 mg/dl increase; 95% confidence interval 0.35 to 0.92; p = 0.02). Internal borderzone infarcts suggestive of haemodynamic causes were the most frequent DWI pattern in patients with MCA occlusion, whereas territorial infarcts suggesting plaque ruptures were most common in those with carotid occlusion. Conclusions: Our results indicate that inflammatory markers, rather than conventional risk factors, reveal clinical and radiological differences between patients with carotid and MCA atherosclerosis. Plaques associated with MCA atherosclerosis may be more stable than those associated with carotid atherosclerosis. PMID:16024892

  18. Evaluation of Early Atherosclerosis Markers in Patients with Inflammatory Bowel Disease

    PubMed Central

    Üstün, Yusuf; Kilincalp, Serta; Çoban, Şahin; Coşkun, Yusuf; Yüksel, İlhami; Ongun, Aydan; Soykan, İrfan; Bektaş, Mehmet; Törüner, Murat; Çetinkaya, Hülya; Örmeci, Necati

    2016-01-01

    Background The aim of this study was to investigate relationships between early atherosclerosis and inflammatory bowel disease (IBD) using laboratory, functional, and morphological markers of atherosclerosis. Material/Methods In the present prospective single-center study, 96 patients with IBD (58 patients with ulcerative colitis and 36 patients with Crohn’s disease) and 65 healthy control subjects were included. The demographic data of each patient and control subject were recorded. The patients with IBD and healthy controls were compared in terms of the carotid intima-media thickness (CIMT), the values of flow-mediated dilatation (FMD) and nitroglycerine-mediated dilatation (NMD), and the levels of von Willebrand factor antigen (VWF-Ag), D-dimer, and lipoprotein (a). Results There were no significant differences between the IBD patients and controls in terms of age, sex, BMI, systolic and diastolic BPs, serum levels of total cholesterol, low-density lipoprotein, or triglycerides. IBD patients had significantly higher levels of VWF-Ag (156.6±58.9 vs. 104.2±43.3, P<0.001) and D-dimer (337.2±710.8 vs. 175.9±110.9, P<0.001) as compared to the controls. No significant differences were determined between the 2 groups in terms of FMD and NMD values. Although statistically not significant, the CIMT values were higher in the IBD patients than in the controls (0.517±0.141 mm vs. 0.467±0.099 mm, P=0.073). In the correlation analysis, the CIMT was found to be correlated negatively with FMD and positively with high sensitive C-reactive protein, VWF-Ag, and D-dimer. Conclusions These findings suggest that VWF-Ag and D-dimer can be beneficial early atherosclerosis markers in IBD patients. PMID:27773920

  19. Long-term macrolide treatment of chronic inflammatory airway diseases: risks, benefits and future developments.

    PubMed

    Cameron, E J; McSharry, C; Chaudhuri, R; Farrow, S; Thomson, N C

    2012-09-01

    Macrolide antibiotics were discovered over 50 years ago and following their use as antimicrobials it became apparent that this group of antibiotics also possessed anti-inflammatory properties. Subsequent clinical trials showed benefits of macrolides as long-term adjuncts in the treatment of a spectrum of chronic inflammatory respiratory diseases, particularly diffuse panbronchiolitis, cystic fibrosis, post-transplant bronchiolitis obliterans and more recently chronic obstructive pulmonary disease (COPD). The evidence for efficacy of macrolides in the long-term treatment of chronic asthma and bronchiectasis is less well established. The mechanism(s) of action of macrolides in the treatment of these diseases remains unexplained, but may be due to their antibacterial and/or anti-inflammatory actions, which include reductions in interleukin-8 production, neutrophil migration and/or function. Macrolides have additional potentially beneficial properties including anti-viral actions and an ability to restore corticosteroid sensitivity. The increased prescribing of macrolides for long-term treatment could result in the development of microbial resistance and adverse drug effects. New macrolides have been developed which do not possess any antimicrobial activity and hence lack the ability to produce microbial resistance, but which still retain immunomodulatory effects. Potentially novel macrolides may overcome a significant barrier to the use of this type of drug for the long-term treatment of chronic inflammatory airway diseases.

  20. Anti-inflammatory modulation of chronic airway inflammation in the murine house dust mite model.

    PubMed

    Ulrich, Kristina; Hincks, Jennifer S; Walsh, Roddy; Wetterstrand, E M Caroline; Fidock, Mark D; Sreckovic, Sasha; Lamb, David J; Douglas, Garry J; Yeadon, Michael; Perros-Huguet, Christelle; Evans, Steven M

    2008-08-01

    Asthma affects 300 million people worldwide and continues to be a major cause of morbidity and mortality. Disease relevant animal models of asthma are required for benchmarking of novel therapeutic mechanisms in comparison to established clinical approaches. We demonstrate that chronic exposure of mice to house dust mite (HDM) extract results in allergic airway inflammation, that can be significantly attenuated by therapeutic intervention with phosphodiesterase 4 inhibition and corticosteroid treatment. Female BALB/c mice were administered intranasally with HDM (Dermatophagoides pteronyssinus) extract daily for five weeks, and therapeutic intervention with anti-inflammatory treatment (dexamethasone 1 mg/kg subcutaneous once daily, prednisolone 10mg/kg orally twice daily, fluticasone 3, 10 and 30 microg intranasally twice daily, roflumilast 10 mg/kg orally twice daily and intranasally 10 and 30 microg twice daily) was initiated after three weeks of exposure. Chronic HDM extract exposure resulted in significant airway inflammation, demonstrated by bronchoalveolar lavage cell infiltration and lung tissue inflammatory gene expression by TaqMan low density array. Chronic steroid treatment significantly inhibited these parameters. In addition, roflumilast caused a significant reduction in airway inflammatory cell infiltration. We have demonstrated that chronic HDM-induced allergic inflammation can be significantly ameliorated by steroid treatment, and that phosphodiesterase 4 inhibition modulates inflammatory cell infiltration. Therefore, the murine HDM model may be a useful tool for evaluating new targets for the treatment of asthma.

  1. [Ultrasonography in chronic inflammatory rheumatic and connective tissue disorders].

    PubMed

    Mérot, O; Le Goff, B

    2014-08-01

    Musculoskeletal ultrasonography is now widely used by almost all rheumatologists thanks to an improvement in the quality of ultrasound unit and probe and to the systematic teaching of this imaging technique to the rheumatology fellows. Applications have broadened from the study of degenerative and mechanical diseases to inflammatory rheumatic diseases. Ultrasound is more sensitive than clinical examination. Power Doppler allows the direct visualisation of inflammation within the tissues. Finally, it is a prognostic tool helping the physician in the management of the disease. This review will focus on the value and applications of ultrasonography in the 2 most frequent rheumatic diseases: rheumatoid arthritis and spondyloarthritis. We will also give some recent data on the usefulness of this imaging technique in the study of musculoskeletal manifestations associated with connective tissue disease.

  2. Improvement of blood inflammatory marker levels in patients with hypothyroidism under levothyroxine treatment.

    PubMed

    Marchiori, Roseane C; Pereira, Luiz A F; Naujorks, Alexandre A; Rovaris, Diego L; Meinerz, Daiane F; Duarte, Marta M M F; Rocha, João B T

    2015-06-23

    < 0.0001), INF-γ (P < 0.0001) and TNF-α (P < 0.0001). No significant difference in hs-CRP over time was observed (P < 0.284). There was a significant reduction in NP-SH (P < 0.0001). This study observed significant changes in the inflammatory profile in hypothyroid patients under treatment, with reduction of pro-inflammatory cytokines and elevation of anti-inflammatory cytokine. In these patients, a decrease in low-grade chronic inflammation may have clinical relevance due to the known connection between chronic inflammation, atherosclerosis and cardiovascular events.

  3. Nutritional markers in patients undergoing chronic haemodialysis in Jamaica.

    PubMed

    Dewar, D; Soyibo, A K; Barton, E N

    2012-06-01

    The main objective of the study is to assess the nutritional status in patients on chronic haemodialysis in Jamaica using the Subjective Global Assessment tool and to correlate this with measured serum nutritional biomarkers, and also to identify nutritional biomarkers that can be used to assess nutritional status of patients with end-stage renal disease (ESRD). Two hundred and nine consecutive patients on haemodialysis were selected from dialysis centres in Kingston, the capital of Jamaica, St. Catherine and Manchester Jamaica. The nutritional status of each participant was assessed using the Subjective Global Assessment tool in an interview performed by the researcher. Serum albumin, blood urea nitrogen and creatinine, highly sensitive complement reactive protein (hsCRP) and total fasting cholesterol were determined from a single serum sample. Only patients with ESRD were selected. Patients with acute renal failure or those with ESRD who were admitted in the previous two weeks were excluded from the study. Informed consent was obtained prior to interview and obtaining blood samples. Of the total participants, 54.5% (n=114) were male and 45.5% (n=95) female. The mean age for males was 51.9 years and females 47.6 years. Diabetes was documented as the most common cause of chronic renal disease and was found in 29.7%, hypertension in 24.4% and chronic glomerulonephritis in 22% of the participants. Approximately 80% of the study population had moderate malnutrition. There was a significant association between moderate malnutrition and a diagnosis of ESRD secondary to diabetes mellitus, p = 0.03. Being on haemodialysis for < or = six months was significantly associated with moderate malnutrition p = 0.002. Also associated with moderate malnutrition were presence of an arteriovenous (AV) fistula (p = 0.01), serum albumin of < 40 g/L (OR 3.68, p = 0.001), pre-dialysis creatinine of <880 micromol/L (p = 0.02) and cholesterol < 3.9 mmol/L (p = 0.04). Highly sensitive

  4. Quantitative analysis of the cellular inflammatory response against biofilm bacteria in chronic wounds.

    PubMed

    Fazli, Mustafa; Bjarnsholt, Thomas; Kirketerp-Møller, Klaus; Jørgensen, Anne; Andersen, Claus Bøgelund; Givskov, Michael; Tolker-Nielsen, Tim

    2011-01-01

    Chronic wounds are an important problem worldwide. These wounds are characterized by a persistent inflammatory stage associated with excessive accumulation and elevated cell activity of neutrophils, suggesting that there must be a persistent stimulus that attracts and recruits neutrophils to the wound. One such stimulus might be the presence of bacterial biofilms in chronic wounds. In the present study, biopsy specimens from chronic venous leg ulcers were investigated for the detection of bacteria using peptide nucleic acid-based fluorescence in situ hybridization (PNA-FISH) and confocal laser scanning microscopy. The bacteria in the wounds were often situated in large aggregates. To obtain a measure of the cellular inflammatory response against the bacteria in the chronic wounds, the amount of neutrophils accumulated at the site of infection was evaluated through differential neutrophil counting on the tissue sections from wounds containing either Pseudomonas aeruginosa or Staphylococcus aureus. The P. aeruginosa-containing wounds had significantly higher numbers of neutrophils accumulated compared with the S. aureus-containing wounds. These results are discussed in relation to the hypothesis that the presence of P. aeruginosa biofilms in chronic wounds may be one of the main factors leading to a persistent inflammatory response and impaired wound healing.

  5. Identification of Novel Anti-inflammatory Agents from Ayurvedic Medicine for Prevention of Chronic Diseases

    PubMed Central

    Aggarwal, Bharat B.; Prasad, Sahdeo; Reuter, Simone; Kannappan, Ramaswamy; Yadev, Vivek R.; Park, Byoungduck; Kim, Ji Hye; Gupta, Subash C.; Phromnoi, Kanokkarn; Sundaram, Chitra; Prasad, Seema; Chaturvedi, Madan M.; Sung, Bokyung

    2011-01-01

    Inflammation, although first characterized by Cornelius Celsus, a physician in first Century Rome, it was Rudolf Virchow, a German physician in nineteenth century who suggested a link between inflammation and cancer, cardiovascular diseases, diabetes, pulmonary diseases, neurological diseases and other chronic diseases. Extensive research within last three decades has confirmed these observations and identified the molecular basis for most chronic diseases and for the associated inflammation. The transcription factor, Nuclear Factor-kappaB (NF-κB) that controls over 500 different gene products, has emerged as major mediator of inflammation. Thus agents that can inhibit NF-κB and diminish chronic inflammation have potential to prevent or delay the onset of the chronic diseases and further even treat them. In an attempt to identify novel anti-inflammatory agents which are safe and effective, in contrast to high throughput screen, we have turned to “reverse pharmacology” or “bed to benchside” approach. We found that Ayurveda, a science of long life, almost 6000 years old, can serve as a “goldmine” for novel anti-inflammatory agents used for centuries to treat chronic diseases. The current review is an attempt to provide description of various Ayurvedic plants currently used for treatment, their active chemical components, and the inflammatory pathways that they inhibit. PMID:21561421

  6. Formula milk feeding does not increase the release of the inflammatory marker calprotectin, compared to human milk.

    PubMed

    Rosti, L; Braga, M; Fulcieri, C; Sammarco, G; Manenti, B; Costa, E

    2011-01-01

    Calprotectin is a protein released into stools, used as a marker of inflammation in inflammatory bowel diseases. We tested the hypothesis that cow's milk protein in formula milk may increase the intestinal release of calprotectin, as a consequence of a subclinical inflammatory reaction. At 12 weeks of age, we measured fecal calprotectin by an immunoenzyme assay (Calprest, Eurospital, Trieste, Italy), in 38 exclusively breastfed and in 32 exclusively formula-fed infants. Fecal calprotectin levels were not different in the two groups (p = 0.09), although a trend to higher values in infants with colic, or with family history of allergies was noted. This suggest that, in general, formula milk does not promote activation of an intestinal inflammatory reaction, compared to human milk, although a subclinical activation of the inflammatory response in infants at risk for allergic diseases may be present.

  7. Characterization of Inflammatory Response in Acute-on-Chronic Liver Failure and Relationship with Prognosis

    PubMed Central

    Solé, Cristina; Solà, Elsa; Morales-Ruiz, Manuel; Fernàndez, Guerau; Huelin, Patricia; Graupera, Isabel; Moreira, Rebeca; de Prada, Gloria; Ariza, Xavier; Pose, Elisa; Fabrellas, Núria; Kalko, Susana G.; Jiménez, Wladimiro; Ginès, Pere

    2016-01-01

    ACLF is characterized by a systemic inflammatory response, but the cytokines involved in this process have not been well studied. The aim of this study was to characterize the systemic inflammatory response in patients with cirrhosis and ACLF and its relationship with prognosis. Fifty-five patients with cirrhosis, 26 with ACLF, were studied prospectively. Systemic inflammatory response was analyzed by measuring a large array of plasma cytokines by using a multiplex kit. A principal component analysis show noticeable differences between ACLF and decompensated cirrhosis without ACLF. Patients with ACLF had significant abnormal levels of 12 cytokines compared to those without ACLF, including: VCAM-1, VEGF-A, Fractalkine, MIP-1α, Eotaxin, IP-10, RANTES, GM-CSF, IL-1β, IL-2, ICAM-1, and MCP-1. Cytokines showing the most marked relationship with ACLF were VCAM-1 and VEGF-A (AUCROC 0.77; p = 0.001). There was a significant relationship between some of inflammatory mediators and 3-month mortality, particularly VCAM-1, ICAM-1, and GM-CSF (AUCROC>0.7; p < 0.05). Functional Enrichment Analysis showed that inflammatory markers differentially expressed in ACLF patients were enriched in leukocyte migration, particularly monocytes and macrophages, and chemotaxis pathways. In conclusion, ACLF is characterized by a marked inflammatory reaction with activation of mediators of adhesion and migration of leukocytes. The intensity of the inflammatory reaction correlates with prognosis. PMID:27578545

  8. The Effects of Body Acupuncture on Obesity: Anthropometric Parameters, Lipid Profile, and Inflammatory and Immunologic Markers

    PubMed Central

    Abdi, Hamid; Zhao, Baixiao; Darbandi, Mahsa; Ghayour-Mobarhan, Majid; Tavallaie, Shima; Rahsepar, Amir Ali; Parizadeh, Seyyed Mohammad Reza; Safariyan, Mohammad; Nemati, Mohsen; Mohammadi, Maryam; Abbasi-Parizad, Parisa; Darbandi, Sara; Akhlaghi, Saeed; Ferns, Gordon A. A.

    2012-01-01

    A randomized controlled clinical trial in 196 obese subjects