Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P05231 (interleukin-6)
 23,907 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Possible correlations between adiponectin, leptin, CD146, a novel adhesion molecule localized at the endothelial junction, and other markers of endothelial cell injury, von Willebrand factor, thrombomodulin, vascular cell adhesion molecule, and intracellular adhesion molecule, and markers of inflammation, tumor necrosis factor-alpha, interleukin-6, and high-sensitivity C-reactive protein in nondiabetic hemodialyzed patients with and without coronary artery disease were studied. Markers of endothelial dysfunction were elevated in hemodialyzed patients, predominantly with coronary artery disease. In multivariate analysis, kinetic urea modeling and plasminogen activator inhibitor-1 remained the only positive predictors of adiponectin. In multivariate analysis, predictors of leptin were triglycerides, tissue plasminogen activator, CD146, and coronary artery disease. In multivariate analysis, predictors of CD146 were age, hemoglobin, and adiponectin. Elevated adiponectin correlated to CD146 may be the expression of a counterregulatory response aimed at mitigating the consequences in endothelial damage and increased cardiovascular risk in renal failure. The data provide further support for a link between adipocytokines, endothelial dysfunction, cardiovascular risk, and renal failure.
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PMID:Adipokines, linking adipocytes and vascular function in hemodialyzed patients, may also be possibly related to CD146, a novel adhesion molecule. 1816 May 86

The aim of this study was to analyze the effect of 2 antiplatelet regimens on the inhibition of GP IIb/IIIa-dependent platelet activation and their association with the poststenting inflammatory response. Seventeen patients with acute myocardial infarction were divided into 2 groups: (A) clopidogrel plus tirofiban infusion administered together during inclusion (n = 10); (B) clopidogrel administered at inclusion and followed 2 hours after by tirofiban (n = 7). Blood samples were obtained at inclusion and at 24 and 48 hours after stenting. Before stenting, a greater reduction of GP IIb/IIIa-dependent platelet activation was found in both groups, although it was greater in group A than in group B. This statistical difference was not observed at 24 and 48 hours after the procedure. At 48 hours after stenting, interleukin-6, interleukin-10, soluble intracellular adhesion molecule-1, and soluble CD40 ligand plasma values were not different between experimental groups. By proteomics, different isoforms of the following proteins were identified: alpha 1-antitrypsin (ATT-1), fibrinogen gamma chain, apolipoprotein A-IV, apolipoprotein A-I, vitamin D binding protein, haptoglobin, and serotransferrin. At 48 hours after stenting, only the plasma expression of the ATT-1 isoform 5 was significantly increased in group A compared with group B. In conclusion, a greater inhibition of GP IIb/IIIa-dependent platelet activation before stenting was not correlated with a different inflammatory activity early after stenting.
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PMID:Effects of coronary prestenting platelet inhibition on coronary poststenting inflammation. 1835 94

Allergic diseases such as asthma and allergic dermatitis are associated with the degranulation of mast cells. Chymase, a mast-cell-specific protease, is the major component in mast cell granules that can induce eosinophil infiltration into inflammatory sites. We examined the immunopathological mechanisms for the activation of eosinophils by chymase in allergic inflammation. Cytokines were measured by cytometric bead array Flex Sets multiplex assay using flow cytometry and enzyme-linked immunosorbent assay. Adhesion molecules, migration and intracellular signalling pathways were assessed by flow cytometry, Boyden chamber assay and Western blot, respectively. Chymase suppressed the apoptosis of eosinophils and induce the release of the cytokine interleukin-6 (IL-6) and chemokines CXCL8, CCL2 and CXCL1 by eosinophils dose-dependently. It also up-regulated the surface expression of adhesion molecule CD18 and stimulated the chemokinetic migration of eosinophils. The expressions of adhesion molecules, cytokines and chemokines, and chemokinetic migration were differentially regulated by the activation of extracellular signal-regulated kinase, p38 mitogen-activated protein kinase, Akt, Janus-activated kinase and nuclear factor-kappaB pathways. Chymase therefore plays a pivotal immunological role in the interaction between mast cells and eosinophils in allergic diseases such as allergic dermatitis by inducing adhesion molecule-mediated chemokinetic migration and inflammatory cytokines and chemokines of eosinophils, through multiple intracellular signalling molecules and transcription factor. Our results therefore provide a further biochemical basis for the pathogenesis of allergic inflammation consequent on the interaction between mast cells and eosinophils, and give insight for the development of new therapies.
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PMID:Signalling mechanisms regulating the activation of human eosinophils by mast-cell-derived chymase: implications for mast cell-eosinophil interaction in allergic inflammation. 1877 39

Higher levels of inflammation are associated with adverse outcomes in patients with lower extremity peripheral arterial disease (PAD). This study evaluated associations of physical activity during daily life with levels of inflammatory biomarkers, D-dimer, and homocysteine in patients with PAD. Participants were 244 men and women (mean age 74.4 +/- 8.2 years) with PAD (ankle brachial index <0.90). C-reactive protein, interleukin-6, soluble intracellular adhesion molecule-1, soluble vascular cellular adhesion molecule-1, D-dimer, and homocysteine were assessed at study entry. Physical activity was objectively assessed with a vertical accelerometer, which participants wore continuously for 7 days. After adjusting for age, gender, race, body mass index, smoking, co-morbidities, ankle brachial index, and other potential confounders, higher physical activity levels were associated linearly and significantly with lower levels of all measured circulating biomarkers: soluble vascular cellular adhesion molecule-1 (p trend = 0.001), D-dimer (p trend = 0.005), homocysteine (p trend = 0.006), interleukin-6 (p trend = 0.010), C-reactive protein (p trend = 0.028), and soluble intracellular adhesion molecule-1 (p trend = 0.033). In conclusion, higher levels of physical activity were associated independently with lower levels of inflammatory markers, homocysteine, and D-dimer in patients with PAD.
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PMID:Physical activity during daily life and circulating biomarker levels in patients with peripheral arterial disease. 1894 Mar 4

Statins exert beneficial effects in chronically damaged tissues. Angiotensin II (ANG II) participates in liver fibrogenesis by inducing oxidative stress, inflammation, and transforming growth factor-beta1 (TGF-beta1) expression. We investigate whether atorvastatin modulates ANG II-induced pathogenic effects in the liver. Male Wistar rats were infused with saline or ANG II (100 ng kg(-1) min(-1)) for 4 wk through a subcutaneous osmotic pump. Rats received either vehicle or atorvastatin (5 mg kg(-1) day(-1)) by gavage. ANG II infusion resulted in infiltration of inflammatory cells (CD43 immunostaining), oxidative stress (4-hydroxynonenal), hepatic stellate cells (HSC) activation (smooth muscle alpha-actin), increased intercellular adhesion molecule (ICAM-1), and interleukin-6 hepatic gene expression (quantitative PCR). These effects were markedly blunted in rats receiving atorvastatin. The beneficial effects of atorvastatin were confirmed in an additional model of acute liver injury (carbon tetrachloride administration). We next explored whether the beneficial effects of atorvastatin on ANG II-induced actions are also reproduced at the cellular level. We studied HSC, a cell type with inflammatory and fibrogenic properties. ANG II (10(-8)M) stimulated cell proliferation, proinflammatory actions (NF-kappaB activation, ICAM-1 expression, interleukin-8 secretion) as well as expression of procollagen-alpha(1(I)) and TGF-beta1. All of these effects were reduced in the presence of atorvastatin (10(-7)M). These results indicate that atorvastatin attenuates the pathogenic events induced by ANG II in the liver both in vivo and in vitro. Therefore, statins could have beneficial effects in conditions characterized by hepatic inflammation.
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PMID:Atorvastatin attenuates angiotensin II-induced inflammatory actions in the liver. 1905 67

Visfatin, a ubiquitous adipokine, was first described in 2005. It was found to be selectively up-regulated in the adipose tissue and to have insulin-mimetic effects. It has been reported that visfatin is associated with endothelial damage in chronic kidney disease. We investigated plasma visfatin levels (using commercially available kits) in 100 clinically stable kidney allograft recipients. We assessed visfatin markers of coagulation: thrombin-antithrombin complexes, prothrombin fragments 1 + 2; fibrinolysis: tissue plasminogen activator, plasminogen activator inhibitor, plasmin-antiplasmin complexes; endothelial function/injury: von Willebrand factor, thrombomodulin, intracellular adhesion molecule, vascular cell adhesion molecule (VCAM); inflammation: hsCRP and interleukin-6. Visfatin was significantly higher in kidney allograft recipients than in healthy volunteers. Visfatin did not differ significantly between diabetic and nondiabetics, hypertensives and normotensives, patients with and without coronary artery disease, and between male and female subjects. Type of immunosuppressive regimen (mycophenolate mofetil vs azathioprine) did not affect visfatin levels. On univariate analysis, visfatin correlated positively with prothrombin fragments 1 + 2, VCAM, creatinine, high-sensitivity C-reactive protein, and negatively with albumin. In multivariate analysis, only VCAM was associated with visfatin in kidney allograft recipients. Visfatin, which is related to markers of inflammation, may represent a novel link between inflammation and adipocytokines among long-term kidney transplant recipients.
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PMID:Visfatin, a new adipocytokine, is predominantly related to inflammation/endothelial damage in kidney allograft recipients. 1924

Numerous studies have found that depression was a strong independent risk factor for incident coronary heart disease (CHD), with increasing risk in those with higher levels of depressive symptoms. The association between measures of inflammation (C-reactive protein, interleukin-6, and soluble intracellular adhesion molecule-1), depressive symptoms, and CHD incidence was examined in 1,794 subjects of the population-based Canadian Nova Scotia Health Survey. There were 152 incident CHD events (8.5%; 141 nonfatal, 11 fatal) during the 15,514 person-years of observation (incidence rate 9.8 events/1,000 person-years). Depression and inflammation were correlated at baseline and each significantly predicted CHD in separate models. When both risk factors were in the same model, each remained significant. The association between depressed group by the Center for Epidemiological Studies-Depression scale (score > or =10 vs 0 to 9) and CHD incidence (hazard rate 1.60, 95% confidence interval 1.12 to 2.27) was not reduced by the addition of inflammatory markers to the model (hazard rate 1.59, 95% confidence interval 1.12 to 2.26). Findings were similar after adjustment for aspirin, lipid-lowering medication, or antidepressant use, and the association did not vary by gender, smoking status, age, obesity, cardiovascular medication use, or antidepressant use. In conclusion, increased inflammation explained only a very small proportion of the association between depression and incident CHD.
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PMID:Relation of inflammation to depression and incident coronary heart disease (from the Canadian Nova Scotia Health Survey [NSHS95] Prospective Population Study). 1926 27

Many potential brain trauma biomarkers have been reported, but no previous study has described outcome prediction using combinations of biomarker levels. We aimed to investigate the outcome predictive values of multiple biomarkers from different mediator families and to determine whether combinations of two serum biomarkers may achieve higher outcome predictive values than individual biomarker levels. A prospective observational study was conducted involving 28 children requiring intensive care management following brain trauma. Day 1 post-injury serum concentrations of eight different biomarkers--S100b protein (S100b), neuron-specific enolase (NSE), interleukin-6 (IL-6), interleukin-8 (IL-8), interleukin-10 (IL-10), soluble intracellular adhesion molecule (SICAM), L-selectin, and endothelin--were quantified using enzyme-linked immunosorbent assay (ELISA). Global outcome was assessed at 6 months post-injury using the Glasgow Outcome Score (GOS). Receiver operator characteristic curve (ROC) analysis and its multivariate extension, Multivariate ROC (MultiROC), were used to assess the outcome predictive values of the individual and the paired biomarkers. None of the eight biomarkers assessed individually achieved an area under the ROC curve (AUC) of more than 0.95 for predicting unfavorable outcome, but five of the 20 biomarker pairs assessed had this high degree of outcome predictability. Two combinations using S100b as the "screening marker" and either L-selectin or IL-6 as the "varying marker" achieved an AUC of 0.98, and their specificity and sensitivity for unfavorable outcome prediction were 96% and 100%, respectively. Prognostic pairs combining serum levels of two biomarkers (inflammatory mediators and brain-specific proteins) offer better outcome predictive values for unfavorable outcome after childhood brain trauma than may be achieved using individual marker levels.
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PMID:Pediatric brain trauma outcome prediction using paired serum levels of inflammatory mediators and brain-specific proteins. 1927 69

Postprandial lipemia (PPL) is associated with impaired endothelial function and inflammation. Acute exercise reduces PPL in adults. This investigation examined the effect of an acute bout of exercise on postprandial changes in triglycerides (TG), glucose, insulin, inflammation [white blood cell count (WBC), interleukin-6 (IL-6) tumor necrosis factor-alpha, C-reactive protein (CRP)] and endothelial activation [soluble intercellular adhesion molecule-1 (sICAM-1), vascular adhesion molecule-1 (sVCAM-1)] following a high-fat meal in adolescents. Ten normal weight (NW) (BMI, 20.9 +/- 1.7 kg m(-2); 15.6 +/- 0.7 years) and eight overweight (OW) (BMI, 28.3 +/- 3.6 kg m(-2); 15.9 +/- 0.4 years) adolescent boys underwent two 6-h oral fat tolerance tests (OFTT) separated by 7-10 days. On the evening prior to each OFTT, subjects either rested or completed a treadmill exercise bout (65% V(O)(2max); 600 kcal expended). Exercise reduced (P < 0.01) the postprandial TG area under the curve by approximately 20% in the NW and OW groups. The postprandial glucose and insulin response did not differ between the control and exercise trials or between the NW and OW groups. Circulating leukocytes and plasma IL-6 levels increased (P < 0.01) in the NW and OW groups 6 h following the OFTT in both experimental conditions. There were no changes in CRP, sVCAM-1 or sICAM-1 following the OFTT and there were no differences between experimental condition or NW and OW groups. In conclusion, a moderate exercise bout prior to a high-fat meal effectively reduces postprandial TG concentrations to a similar degree in both NW and OW adolescents, but does not reduce the concomitant postprandial increase in WBC or IL-6.
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PMID:Effect of prior exercise on postprandial lipemia and markers of inflammation and endothelial activation in normal weight and overweight adolescent boys. 1970 68

The metabolic syndrome is associated with insulin resistance, a systemic low-grade inflammatory state, and endothelial dysfunction. These disorders may arise at a very early age in obese children. The aim of this study was to confirm changes in endothelial dysfunction and inflammatory biomarkers in obese prepubertal children and to evaluate the effect of body mass index (BMI) modification on these biomarkers. Biomarkers for inflammation, endothelial dysfunction, and insulin resistance were measured in obese children (47) and healthy controls (47). Baseline pretreatment levels of insulin (P = .019), homeostasis model assessment of insulin resistance (P = .004), soluble intercellular adhesion molecule (sICAM) (P = .003), and C-reactive protein (CRP) (P < .001) were significantly higher in obese children than in controls. After 9 months of treatment, obese children with lowered BMI SD score (SDS-BMI) displayed a significant decrease in insulin (P = .011), homeostasis model assessment of insulin resistance (P = .012), CRP (P = .006), and interleukin-6 (IL-6) (P = .045) levels compared with obese children with stable SDS-BMI; they also displayed a nonsignificant drop in sICAM levels. Similarly, obese children with lowered SDS-BMI displayed a decrease in CRP (P = .005) and IL-6 (P = .065) compared with baseline levels before treatment. In the total obese group, changes in SDS-BMI correlated positively with changes in CRP (P = .035), IL-6 (P = .027), and sICAM-1 (P = .038) levels. Only SDS-BMI was an independent predictive factor for CRP (P = .031), IL-6 (P = .027), and sICAM-1 (P = .033). Prepubertal obese children displayed alterations indicative of endothelial dysfunction, insulin resistance, and inflammatory state. Lowering of the SDS-BMI after 9 months of treatment was associated with an improvement in these variables compared with those in obese children with stable SDS-BMI status.
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PMID:Changes in body mass index are associated with changes in inflammatory and endothelial dysfunction biomarkers in obese prepubertal children after 9 months of body mass index SD score loss. 1947 72


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