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)

During end-stage heart failure, plasma levels of interleukin-6 (IL6) are elevated. This cytokine exerts a negative inotropic influence on the myocardium. The production site of IL6 is unclear. We examined the hypothesis that IL6 in end-stage heart-failure patients is produced in the myocardium itself and is differentially regulated according to etiology. Cardiac tissue was obtained from 27 patients (idiopathic dilated cardiomyopathy, (DCM) 9/6 m/f, age 46 +/- 14 y; ischemic cardiomyopathy (ICM), 11/1 m/f, age 55 +/- 8 y) at the time of transplantation. The tissue was subjected to IL6 Northern-blot analysis. Signals were quantified by densitometric scanning after normalization to G3 PDH mRNA. Data were compared by Mann-Whitney test between DCM and ICM patients, divided by chamber origin. IL6 transcripts were found in all patients. In DCM, left-ventricular IL6 mRNA expression was higher than in ICM (p = 0.006). Median right-ventricular as well as left- and right-atrial IL6 mRNA expression was not significantly different in both groups. In summary, in end-stage heart failure, IL6 mRNA is consistently expressed in the myocardium. Left-ventricular expression is higher in DCM than in ICM. These data support the concept of a potentially reversible inflammatory component in the etiology of DCM which is more pronounced than in patients with ICM of comparable clinical severity.
Thorac Cardiovasc Surg 1998 Aug
PMID:Left-ventricular expression of interleukin-6 messenger-RNA higher in idiopathic dilated than in ischemic cardiomyopathy. 977 95

High plasma fibrinogen appears to be an important risk factor for the development of atherosclerosis. The aim of our study was to measure fibrinogen and fibrin degradation products (D-dimer), interleukin-6 tissue plasminogen activator, plasminogen activator inhibitor-1 and urokinase-type plasminogen activator in the plasma and arterial walls of 45 patients who had arterial surgery between April 1993 and November 1995. The arterial specimens were also examined by immunohistochemists for these same factors. The serum fibrinogen and fibrin degradation products were high in all patients, and fibrinolysis was depressed. Few leukocytes were seen in the arterial walls, which had poor fibrinolytic activity. Plasminogen-activator inhibitor activity in the wall was also reduced in the affected arterial walls. The abdominal aorta appeared to have the highest levels of fibrinogen and this may be related to its ability to form aneurysms. Fibrinogen may play an important role in the progression of atherosclerotic disease.
Cardiovasc Surg 1998 Oct
PMID:Fibrinogen and fibrinolysis in blood and in the arterial wall: its role in advanced atherosclerotic disease. 979 64

Disruption of atherosclerotic plaques with associated thrombus is responsible for the majority of the acute coronary syndromes. Plaque instability is related closely to the degree of inflammation. Inflammatory cells within the plaque produce cytokines that inhibit collagen production by vascular smooth muscle cells and increase the production of metalloproteinases, which degrade the extracellular matrix in the fibrous cap. The recruitment of inflammatory cells into the vessel wall occurs in a coordinated sequence of events involving the expression of cellular adhesion molecules on the surface of activated endothelial cells and the production of chemoattractants, and occurs in part in response to oxidation of low-density lipoprotein within the vessel wall. The cellular adhesion molecules are shed into the circulating blood in several disease states, including clinically evident atherosclerosis. The acute-phase reactants C-reactive protein and interleukin-6, and markers of the fibrinolytic state (plasminogen activator inhibitor-1 and tissue plasminogen activator), are also elevated in the acute coronary syndromes and in healthy individuals at increased risk for developing coronary artery disease. These markers may reflect vascular inflammation and thereby the stability of atherosclerotic plaques. Their measurement may pinpoint the mechanisms of benefit of cholesterol-lowering therapy and other interventions designed to reduce coronary risk, and potentially could offer a new method for monitoring coronary risk factor reduction in patients.
J Cardiovasc Pharmacol 1998
PMID:Inflammation, the endothelium, and the acute coronary syndromes. 988 50

We introduced thoracoscopic esophagectomy with extended lymphadenectomy for reduction of respiratory dysfunction and less surgical intervention in July 1995. In this study, we investigated the changes in serum interleukin-6 (IL-6) and interleukin-1 receptor antagonist (IL-1ra) levels in 8 patients (TS Group) who underwent thoracoscopic esophagectomy with extended lymphadenectomy and compared them with the changes in patients who underwent conventional thoracotomy (CT Group). The duration of the operation and intrathoracic procedure in the TS group were significantly longer than in the CT group. However, the amount of blood loss and intrathoracic blood loss of the TS group were not significantly higher than in the CT group. The number of dissected lymph nodes was not significantly larger. The serum IL-6 levels reached maximum levels 3 hours from the end of operation. In the TS group, the changes in IL-6 levels were significantly larger (p < 0.05). On the other hand, the changes in CRP levels were also significantly larger (p < 0.01). Significant correlation was observed between the duration of the intrathoracic procedure and the maximum levels of IL-6. On the other hand, serum IL-1ra levels were not significantly. At present, these results suggest that the surgical intervention of thoracoscopic esophagectomy are more larger than that of conventional thoracotomy. We think that the length of intrathoracic procedure of thoracoscopic esophagectomy may make more large surgical stress.
Jpn J Thorac Cardiovasc Surg 1998 Dec
PMID:[Changes of serum cytokine levels after thoracoscopic esophagectomy]. 1003 40

Heparin-coated cardiopulmonary bypass circuits reduce the inflammatory response to cardiopulmonary bypass circuit, improve biocompatibility and may protect the postoperative hemostasic mechanisms in routine coronary bypass operations. 'High-dose' aprotinin reduces bloodloss, transfusion needs, and re-explorations as a result of bleeding, and may have an additional role in reducing the inflammatory response of the body to cardiopulmonary bypass circuit. It has not been established, however, if the addition of a heparin-coated circuit to the intraoperative administration of 'high dose' aprotinin further reduces the whole-body inflammatory response to cardiopulmonary bypass circuit and improves the postoperative clinical course of the patients who are undergoing coronary surgery. Thirty patients undergoing primary elective coronary artery bypass grafting were studied. All the patients received, intraoperatively, the serine-protease inhibitor aprotinin according to the 'Hammersmith' protocol and full heparin dose. Patients were randomly allocated to be treated either with a circuit completely coated with surface-bound heparin (n = 15) or with an uncoated, but otherwise identical, circuit (n = 15). Differences in the clinical course of the two groups of patients, as well as differences in the behavior of hematological and inflammatory (interleukin-6 (IL-6) and C-reactive protein) factors before, during and after bypass, were analyzed. There were no significant differences between the two groups in terms of bleeding and transfusional requirements, the time spent on a ventilator, or in duration of stay in the intensive care unit (ICU). In all patients, a significant increase in the total white blood cell count, neutrophils, serum IL-6 and C-reactive protein occurred in relation to cardiopulmonary bypass. This was not influenced by heparin precoating of the circuit. In addition, there was an increase in the monocyte count during follow-up, and there was a trend towards higher monocyte counts in the patients who were treated with heparin-coated circuits. These results suggest that the addition of a heparin-coated circuit to the intraoperative 'high-dose' aprotinin therapy probably had little influence on the clinical course and on the time-course of the inflammatory parameters of the adult patients undergoing primary coronary surgery with a full heparinization protocol.
Cardiovasc Surg 1999 Jan
PMID:'High dose' aprotinin and heparin-coated circuits: clinical efficacy and inflammatory response. 1007 71

The adverse effect of neoadjuvant chemoradiotherapy on the postoperative course in esophageal cancer was studied in 9 patients undergoing neoadjuvant chemoradiotherapy preceding surgery for thoracic esophageal carcinoma possibly involving adjacent organs (neoadjuvant group), and 13 patients undergoing surgery without neoadjuvant therapy for same disease (control group). The two groups were compared for volume of intraoperative hemorrhage, surgical duration, frequency of postoperative morbidity, and for postoperative changes in blood platelet counts, and serum thrombopoietin and interleukin-6 levels. Mean intraoperative blood loss was 1121 g (580-1,662 g) in the neoadjuvant group and 546.5 g (274.7-778.3 g) in controls group (Student's T test: p < 0.01). No significant difference was seen found between the two groups in the degree of postoperative deterioration in cardiopulmonary function or in interleukin-6 levels. Blood platelet counts decreased in both groups until postoperative day 7, but recovery on postoperative day 14 was significantly depressed in the neoadjuvant group compared to controls. Serum thrombopoietin levels were higher in the neoadjuvant group than in controls (Mann-Whitney U-test: p < 0.05). We found that neoadjuvant chemoradiotherapy induces latent postoperative myelosuppression and may lead to intractable infection.
Jpn J Thorac Cardiovasc Surg 1999 Jun
PMID:Problems in neoadjuvant chemoradiotherapy preceding surgery for advanced squamous cell carcinoma of the thoracic esophagus. 1042 44

Cardiac myxomas are benign tumors which sometimes secrete interleukin-6 (IL-6), however, the pathogenesis and the IL-6 secreting cells are not clear. There are vascular myosin heavy chain isoforms; SM2 expression is specific to mature smooth muscle cells, while SMemb is a nonmuscle-type isoform which is expressed in immature mesenchyme cells. We hypothesized that immature mesenchyme cells play pivotal roles in the secretion of IL-6; we studied these expression in resected samples of myxoma. SMemb expression was increased but SM2 expression was not in the channels of myxoma. Increased IL-6 transcription was observed in the SMemb expressing cells in the channel. Therefore, mesenchyme cells with immature phenotype in the channel play pivotal roles of inflammation and pathogenesis of cardiac myxoma.
Cardiovasc Pathol
PMID:In situ interleukin-6 transcription in embryonic nonmuscle myosin heavy chain expressing immature mesenchyme cells of cardiac myxoma. 1073 5

Children are sensitive to the inflammatory side effects of cardiopulmonary bypass (CPB). Our intention was to investigate if the biocompatibility benefits of heparin-coated CPB circuits apply to children. In 20 operations, 19 children were randomized to heparin-coated (group HC, n = 10) or standard (group C, n = 10) bypass circuits. Plasma levels of acute phase reactants, interleukins, granulocytic proteins and complement factors were measured. All were significantly elevated after CPB. Levels of complement factor C3a (851 (791-959)ng/ml [median with quartiles] in group C, 497 (476-573)ng/ml in group HC, p < 0.001), Terminal Complement Complex (114 (71-130) AU/ml in group C, 35.5 (28.9-51.4) AU/ml in group HC, p < 0.001), and interleukin-6 (570 (203-743) pg/ml in group C, 168 (111-206)pg/ml in group HC, p = 0.005), were significantly reduced in group HC. Heparin-coated CPB circuits improve the biocompatibility of CPB during heart surgery in the paediatric patient population, as reflected by significantly reduced levels of circulating complement factors and interleukin-6.
Scand Cardiovasc J 2000
PMID:Heparin-coated cardiopulmonary bypass circuits reduce circulating complement factors and interleukin-6 in paediatric heart surgery. 1081 58

Immunosuppression may have an important impact on early graft coronary endothelial injury. We investigated functional and morphologic coronary alterations, myocardial expression, and cardiac release of possible mediators of allograft vasculopathy within 6 months after cardiac transplantation with respect to different immunosuppressive regimens. Epicardial and microvascular endothelium-dependent and endothelium-independent vasomotor function and epicardial intimal thickening were measured in 8 transplant recipients treated with cyclosporin A (CyA), azathioprine, and prednisone (group 1), 9 transplant recipients treated with tacrolimus (TKL), azathioprine, and prednisone (group 2), and 14 patients treated with TKL, mycophenolate mofetil (MMF), and prednisone (group 3). The gene expressions of inducible and endothelial nitric oxide synthase (iNOS and eNOS), endothelin-1, prostacyclinsynthase, and thromboxansynthase were analyzed in endomyocardial biopsy specimens using semiquantitative reverse transcription polymerase chain reaction. Transcardiac cytokine release, endothelin-1, and nitrate-release were determined from plasma samples. Epicardial endothelial dysfunction (vasoconstriction to acetylcholine > 10%) and microvascular smooth muscle cell dysfunction (flow velocity increase to adenosine and nifedipine < 2.0) were enhanced in heart transplant recipients immunosuppressed with TKL, azathioprine, and prednisone. The prevalence of epicardial dysfunction was 78% in group 2 versus 44% and 46% in group 1 and 3 (p < 0.05), respectively. The prevalence of microvascular dysfunction was 56% in group 2 versus 13% and 7% in group 1 and 3 (p < 0.02), respectively. Coronary vasomotor dysfunction was associated with increased myocardial iNOS expression (p < 0.05), decreased eNOS expression (p < 0.05), and enhanced cardiac immunoreactive interleukin-6 (p < 0.01). Coronary intimal thickening was not different between the groups. The combination of TKL and MMF appears to be superior to TKL and azathioprine (and comparable to CyA and azathioprine) concerning preservation of early coronary vasomotor function, eNOS expression, iNOS suppression as well as cardiac interleukin-6 release. This may have an important impact on subsequent development of transplant coronary atherosclerosis.
J Cardiovasc Pharmacol 2000 Dec
PMID:Coronary vasomotor dysfunction in the cardiac allograft: impact of different immunosuppressive regimens. 1111 79

We previously reported that the spillover of interleukin-6 (IL-6) into the peripheral circulation increases with the severity of congestive heart failure (CHF), and that the increase is mainly associated with activation of the endogenous sympathetic nervous system. However, the role of the sympathetic nervous system in the increase of IL-6 in CHF patients is not yet fully understood. To address this question, we measured plasma IL-6 levels before and after therapeutic administration of dopamine and betablockers in patients with CHF. After more than 24 h (mean, 34 h) of treatment with a low dose of intravenous dopamine (mean, 2.4 microg/kg/min) in 1 patients with dilated cardiomyopathy and deterioration of CHF, the plasma IL-6 level was increased significantly (30.8 vs. 16.6 pg/ml; p = 0.003) despite the improved hemodynamics. After 377 days of beta-blocker therapy in 24 patients with dilated cardiomyopathy, the plasma IL-6 level was decreased significantly (2.04 vs. 3.11 pg/ml; p = 0.01) along with the improvement of symptoms, left ventricular ejection fraction, and neurohumoral factors. Dopamine increases and beta-blockers decrease the plasma IL-6 level in patients with CHF, suggesting that drugs modulating the sympathetic nervous system may alter IL-6 in these patients.
J Cardiovasc Pharmacol 2000
PMID:Therapeutic use of dopamine and beta-blockers modulates plasma interleukin-6 levels in patients with congestive heart failure. 1120 29


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