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)

Interleukin-6 (IL-6), a proinflammatory cytokine, plays a key role in the pathogenesis of coronary artery disease (CAD). We investigated circulating IL-6 and its receptors in patients with CAD. We evaluated 39 Japanese patients with CAD (30 males and 9 females aged 36-79 years), measuring their plasma levels of IL-6 and IL-6 receptors alpha and beta (IL-6R alpha, IL-6R beta). Circulating levels of IL-6, IL-6R alpha and IL-6R beta were measured by an enzyme-linked immunosorbent assay. Blood was sampled immediately after admission and again after 1, 2, 3, 6 and 9 h, then every 12 h for 5 days. Atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) were measured on day 3 after symptom onset. Plasma levels of IL-6 and IL-6Rs were significantly increased in 28 patients with acute myocardial infarction (AMI) compared with 15 normal controls. However, neither IL-6 nor IL-6Rs showed an increase in 6 patients with angina pectoris. We observed two peaks for circulating IL-6 in AMI, the first of which showed a significant correlation with ANP as well as BNP. These results may help to explain why the amount of IL-6 produced is closely related to the severity of myocardial dysfunction in patients with CAD.
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PMID:Circulating interleukin-6 and interleukin-6 receptors in patients with acute and recent myocardial infarction. 1096 91

To investigate relationships between thyroid states and the cardiac endocrine system, we analyzed thyrotropin (TSH), thyroid hormone, plasma levels of interleukin-6 (IL-6) and brain natriuretic peptide (BNP) in 50 patients with chronic heart failure (CHF), in 30 patients with heart failure from acute myocardial infarction (AMI), and in 15 controls. Plasma levels of IL-6 and BNP in both CHF and AMI were significantly elevated, while free triiodothyronine (FT3) was significantly decreased compared to controls. FT3/free thyroxine (FT4) ratio was significantly decreased in CHF but not in AMI compared to controls. In CHF, diuretic treatment diminished circulating BNP but not IL-6, while diuretic treatment increased FT3/FT4 ratio. In AMI, FT3/FT4 ratio was significantly decreased 72 h compared to 12 h after the onset of AMI, while BNP and IL-6 were significantly increased 72 h compared to 12 h after the onset of AMI. In both CHF and AMI, BNP significantly correlated with FT4. On the other hand, significant correlations between IL-6 and FT3, and between IL-6 and FT3/FT4 ratio were detected in AMI but not in CHF. This preliminary study suggests that IL-6, BNP and thyroid hormone reflect ventricular dysfunction in both acute and chronic heart failure, and that IL-6 significantly relates to circulating thyroid hormone in AMI but not in CHF.
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PMID:Circulating interleukin-6 significantly correlates to thyroid hormone in acute myocardial infarction but not in chronic heart failure. 1102 66

Background: Interleukin-6 (IL-6) is a key cytokine in the initiation of the acute-phase reaction that accompanies myocardial infarction. The study was designed to evaluate changes in serum IL-6 in patients with myocardial infarction and to compare IL-6 alterations with serum creatine kinase (CK) activity. Methods: Serum IL-6 level and CK activity were measured in 19 males with acute myocardial infarction. Blood was taken on the 1st, 3rd, 5th, 7th and 21st days of the disease. Control values were obtained from 30 age-matched healthy males. IL-6 was determined according to the ELISA method and CK was measured with a routine procedure. Results: Serum IL-6 was found to increase on the 1st and 3rd days of the disease, followed by some decline on days 5-21. However, the last values measured were still higher than those in the controls. Patients with transmural myocardial infarction had higher IL-6 levels than those with non-Q myocardial infarction. There was no difference in serum IL-6 in patients with myocardial infarction of the inferior cardiac wall and of the anterior cardiac wall. A correlation was found between IL-6 level and CK activity in the patients, especially on the 1st and 3rd days of the disease. Conclusion: Serum IL-6 increases in patients with myocardial infarction, and this elevation seems to be related to the mass of the affected myocardium. The highest increase is found during the first days of the disease, although the enhanced IL-6 level lasts for at least 3 weeks, probably reflecting the healing process of the myocardium. The clinical value of IL-6 determination does not seem to exceed that of the indices commonly used.
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PMID:Dynamics of serum interleukin-6 level in patients with acute myocardial infarction. 1102 49

The changes in serum concentrations of cytokines such as interleukin-1 (IL-1) beta, interleukin-6 (IL-6), tumor necrosis factor (TNF) alpha and a soluble-intercellular adhesion molecule (sICAM-1) has been investigated in patients with stable angina and acute myocardial infarction. Thirty-four patients with stable angina (SA), 15 with acute myocardial infarction (AMI), and 20 subjects in the control (C) group were included in the study. The mean serum concentrations of sICAM-1, IL-1-beta, IL-6, and TNF-alpha differed significantly among the three groups. Serum concentrations of IL-1 beta, sICAM-1, and TNF-alpha were comparable in the AMI and SA groups and higher than those found in the C group (p < 0.001). The serum concentration of IL-6 was more than twice as high in the AMI group as compared to the other two groups (p < 0.001). The mean serum concentrations of IL-1 beta, TNF-alpha, and IL-6 were comparable in the AMI and SA groups and higher than in the C group.
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PMID:Circulating interleukin-1 beta, interleukin-6, tumor necrosis factor-alpha, and soluble ICAM-1 in patients with chronic stable angina and myocardial infarction. 1122 83

Cardiotrophin-1 (CT-1) is a recently identified cytokine of the interleukin-6 (IL-6) family that signals through the gp130 signalling pathway. CT-1 may be of central importance to the pathogenesis of ventricular remodelling in patients with acute myocardial infarction (AMI) and therefore have clinical value in the identification of patients with impaired ventricular function. Central to the clinical use of CT-1 is in the in vitro stability of the peptide. Twelve subjects were recruited. A total of 25 mL of peripheral venous blood was collected into chilled polypropylene tubes containing EDTA and aprotinin and divided into 5 aliquots. One sample was spun in a prerefrigerated centrifuge (4 degrees C) at 3,000 rpm for 10 minutes and plasma separated and frozen at -70 degrees C immediately. Remaining samples were stored for 24 and 48 hours at room temperature or on ice. CT-1 in extracted plasma specimens was measured with a competitive chemiluminescent assay. The concentration of CT-1 in samples stored optimally was 43.1 +/- 6.05 fmol/mL. CT-1 levels for storage at room temperature compared with ice at the remaining time points were as follows: 24 hours, 41.5 +/- 5.76 v 37.5 +/- 8.66; and 48 hours, 42.6 +/- 6.28 v 41.0 +/- 5.42 fmol/mL. There were no significant changes in concentrations of CT-1 stored optimally or kept for up to 48 hours in aliquots of whole blood at room temperature or on ice. We conclude that CT-1 is stable in specimens of whole blood treated with EDTA and aprotinin and stored for up to 48 hours at room temperature or on ice, hence permitting its development in the routine clinical investigation of patients with heart failure.
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PMID:Prolonged stability of endogenous cardiotrophin-1 in whole blood. 1122 35

Estimation of cardiac morbidity in patients after major surgery is a difficult problem. In addition, infectious complications seriously decrease potential beneficial outcome after cardiovascular surgery. The present study assessed the use of a newer marker of the inflammatory response, procalcitonin, in the field of myocardial infarction, in conjunction with measurements of interleukin-6. Forty-four consecutive cases with acute myocardial infarction were included in the study 4+/-1.3 h after the onset of symptoms. Plasma levels of procalcitonin and interleukin-6 were obtained at admission, and after 3, 6, 12, 18, 24 and 48 h, using commercially available test kits. The range of levels of interleukin-6 and procalcitonin was about normal at admission. Interleukin-6 levels increased significantly following myocardial infarction, whereas procalcitonin were essentially unchanged, i.e. remained close to the normal level threshold of 0.5 ng/ml; only minor variability occurred with a mean peak level of procalcitonin of 1+/-0.4 ng/ml. Data demonstrate that, in contrast to the acute phase reactant interleukin-6, plasma levels procalcitonin are not significantly elevated during uncomplicated acute myocardial infarction. This observation may support the role of procalcitonin measurements in the differential diagnosis of infectious and cardiovascular complications after major surgery.
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PMID:Plasma levels of procalcitonin and interleukin-6 in acute myocardial infarction. 1132 65

The designation of atherosclerosis as a chronic inflammatory process represents an exciting and logical paradigm shift for cardiologists. Plasma concentrations of interleukin-6 (IL-6) and its hepatic by-product C-reactive protein (CRP) appear to reflect the intensity of occult plaque inflammation and by inference may determine vulnerability to rupture. Indeed, circulating IL-6 levels are elevated in patients with acute myocardial infarction (AMI), and also in patients with unstable, but not with stable angina. Coronary sinus IL-6 concentrations are also increased after percutaneous coronary intervention (PCI), and late restenosis correlates with an increase in IL-6 concentration after the procedure, indicating that IL-6 expression may be not only related to instability of atheromatous plaques, but also to the formation of restenotic lesions after PCI. These observations suggest the advantage of screening for circulating IL-6 concentration and the use of anti-inflammatory treatment for those thought be at high risk to reduce the risk of future AMI.
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PMID:Interleukin-6 and acute coronary syndrome. 1171 26

The aim of this study was to determine the spatial and temporal expression of various pro-inflammatory cytokines in the peri-sinoatrial nodal area after atrial infarction. Rats were subjected to permanent atrial infarction, in particular, sinoatrial node (SAN) infarction and sacrificed at various time points up to 7 days. Real-time polymerase chain reaction analysis demonstrated that mRNA levels of tumor necrosis factor alpha (TNF-alpha), interleukin-1beta, interleukin-6, and transforming growth factor beta 1 (TGF-beta(1)) were upregulated in the peri-sinoatrial nodal area after atrial infarction. Immunostaining for TNF-alpha and TGF-beta(1) proteins revealed that both cytokines were expressed persistently up to 7 days after atrial infarction around the peri-sinoatrial nodal area. Furthermore, the infiltrating inflammatory cells immunoreactive for both cytokines were predominant within the infarct SAN. In situ hybridization analysis showed that TNF-alpha gene expression was enhanced in the inflammatory cells and myocardium within the peri-sinoatrial nodal area in response to the infarction. These results provide evidence for the local expression of cytokines in the post-ischemic peri-sinoatrial nodal area, suggesting that the upregulation of the cytokines might be associated with the atrial arrhythmia observed after acute myocardial infarction.
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PMID:Induction of cytokine expression in rat post-ischemic sinoatrial node (SAN). 1224 84

The physiologic events leading to apoptosis in myocardial infarction and the molecules involved in the death process have not been clarified unequivocally. We developed a method to search for serum factors that induce apoptosis of human cells, using serum obtained from patients within 1 day of the onset of acute myocardial infarction (AMI). Serum factors were found to have the ability to increase the caspase-3 activity levels in human RSa cells, which are susceptible to apoptosis inducers. The factors obtained from AMI patients by elution at about 0.5 mol/L KCl from a dye-ligand column were named AMI-SFs (serum factors from AMI). Electrophoretic analysis showed DNA fragmentation in AMI-SF-treated RSa cells, but not in RSa cells treated with fractions from AMI patients 1 week after clinical onset of illness. AMI-SF-induced DNA fragmentation was also demonstrated by terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling analysis, whereas a suppression of fragmentation was seen in RSa cells treated with AMI-SFs in combination with a caspase-3 inhibitor. The increase in caspase-3 activity was not inhibited by neutralizing antibodies to tumor necrosis factor-alpha, interleukin-6, human interferon-beta, or interferon-gamma. Polymerase chain reaction-based messenger RNA differential display and Northern blotting revealed an increase in the messenger RNA expression level of human ubiquitin hydrolase in AMI-SF-treated RSa cells. Antisense oligonucleotides for ubiquitin hydrolase inhibited the increase in caspase-3 activity. These findings suggested that serum from AMI patients in the acute phase contains factors that induce apoptosis, possibly by inducing the expression of the ubiquitin hydrolase gene, at least in the human cells tested.
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PMID:Induction of apoptosis and ubiquitin hydrolase gene expression by human serum factors in the early phase of acute myocardial infarction. 1262 96

High PAI-1 levels post acute myocardial infarction (AMI) are associated with a poor outcome. Concentrations of insulin-like molecules, proinflammatory cytokines and an insertion (5G)/deletion (4G) polymorphism in the promoter of the PAI-1 gene, all influence circulating PAI-1 levels. We studied the determinants of PAI-1 in 123 patients immediately following and at 6 months after AMI. Within 24 h of AMI, PAI-1 levels were related to those of proinsulin-like molecules but not to levels of cytokines (interleukin-1beta, interleukin-6 or tumour necrosis factor-alpha), to genotype, or to interactions between genotype and cytokine concentration. PAI-1 levels 6 months after AMI were related to concentrations of interleukin-1beta but not to genotype. We have found no evidence that subjects with the 4G/4G polymorphism have higher PAI-1 levels on admission or 6 months after AMI. In these patients, levels of PAI-1 are related to concentrations of proinsulin-like molecules and of proinflammatory cytokines.
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PMID:Plasminogen activator inhibitor-1 (PAI-1) activity post myocardial infarction: the role of acute phase reactants, insulin-like molecules and promoter (4G/5G) polymorphism in the PAI-1 gene. 1280 13


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