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)

To eliminate the cytokines and leukocytes-induced proteases which could cause the multisystem organ failure postoperatively, we performed a preliminary hemodialysis to the priming solution and a continuous hemodialysis during extracorporeal circulation (ECC) in 5 children (HD group), and neither hemodialysis in another 5 children (Control group). We measured the plasma level of Interleukin-1 (IL-1), Interleukin-6 (IL-6) and leukocyte elastase (Ease) to evaluate the efficiency of these hemodialysis. Urine level of alpha 1-microglobulin (MG), beta 2-MG, urine volume, water balance and perfusion pressures during ECC were also measured to evaluate its protective effect for the renal function. IL-1 level significantly decreased in HD group 1 and 12 hours after operation. Not only IL-6 and Ease during ECC but also alpha 1- and beta 2-MG 1 hour after operation decreased in HD group so hemodialysis could be useful to eliminate the cytokines. Ease and could protect the renal function. Water balance and perfusion pressures also obtained good results with these hemodialysis. Plasma osmolality and glucose level changed within the normal range in HD group, conversely over the normal range in control group. We conclude this method is useful for neonatal, ECC.
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PMID:[Efficiency of the preliminary and continuous hemodialysis at open heart surgery in infants and children]. 761 27

The proinflammatory cytokine interleukin-6 (IL-6) and its potential opponent, transforming growth factor-beta (TGF-beta 1), have been discussed as being involved in the regulation of inflammatory processes following trauma and infections. The aim of this study was to investigate the effect of these cytokines on the regulation of neutrophil degranulation. The posttraumatic time courses of the plasma concentrations of IL-6, and the elastase-alpha 1-proteinase-inhibitor complex as marker of degranulation in patients undergoing severe trauma were found to be highly correlated, whereas TGF-beta 1 levels were determined to be not significantly altered. The close temporal correlation of IL-6 and elastase levels could be confirmed by investigation of exudates derived from the surgical area. To prove these in vivo findings, the effect of IL-6 and TGF-beta 1 on the degranulation of isolated neutrophils of healthy donors was investigated in vitro. Pathological high IL-6 concentrations were found to be capable of inducing a significant release of lysosomal elastase in a concentration-dependent manner, whereas the degranulation was unaffected by TGF-beta 1. In conclusion, these data suggest an involvement of IL-6 in the regulation of neutrophil degranulation under pathological conditions. However, TGF-beta 1 seems to have no direct regulatory effects besides its described chemotactic function on neutrophils.
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PMID:Effects of interleukin-6 (IL-6) and transforming growth factor-beta (TGF-beta) on neutrophil elastase release. 770 89

To infer possible mechanisms of acute airway inflammation and mucus hypersecretion in acute severe asthma, we performed cellular and biochemical analysis on sputum from 18 adults with acute severe asthma and compared the results with results of analysis of sputum from 12 adults with cystic fibrosis (CF). We found that in subjects with asthma neutrophils made up more than 75% of sputum cells in 10 samples whereas eosinophils made up more than 75% of cells in only three samples. Fifty percent of the subjects with asthma reported that their asthma exacerbation was precipitated by a respiratory tract infection, and these subjects had a significantly higher percentage of neutrophils in their sputum (85% +/- 6% vs 57% +/- 12%, p = 0.05). In the CF samples neutrophils made up more than 95% and eosinophils less than 1% of cells in all samples analyzed. Analysis of fluid phase chemicals in asthmatic and CF sputum samples showed that despite overall lower mean values of neutrophil elastase (27 +/- 11 micrograms/ml vs 466 +/- 121 micrograms/ml, p = 0.0001) and interleukin-8 (IL-8) (55 +/- 15 ng/ml vs 186 +/- 24 ng/ml, p = 0.0001), some of the asthmatic samples had values for these variables that overlapped those in the CF samples. In addition, the asthmatic samples were distinguished by the presence of higher tryptase (10 +/- 7 U/L vs 0.9 +/- 0.9 U/L, p = 0.0001) and interleukin-6 (1166 +/- 447 ng/ml vs 186 +/- 24 ng/ml; p = 0.0001) levels and by a higher ratio of albumin to mucin-like glycoprotein (0.8 +/- 0.5 vs 0.1 +/- 0.002, p = 0.02). DNA levels were lower in the asthmatic samples (0.5 +/- 0.3 mg/ml vs 3.5 +/- 1.2 mg/ml, p = 0.05). We conclude that neutrophils predominate more frequently than eosinophils as the major inflammatory cell in sputum from patients with asthma in acute exacerbation. We speculate that this may be because respiratory tract infections are a frequent precipitant of acute asthma. In addition, the high IL-8 levels and free neutrophil elastase activity observed in asthmatic sputum suggests that IL-8 may mediate airway neutrophilia in acute asthma and that neutrophil elastase may mediate mucin glycoprotein hypersecretion in acute asthma, as has been proposed for the mucin hypersecretion in CF.
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PMID:Prominent neutrophilic inflammation in sputum from subjects with asthma exacerbation. 772 65

In this study we investigated the interleukin-8 concentration (IL-8) and granulocyte elastase activity (GE) after elective abdominal surgery. Postoperative interleukin-6 (IL-6), IL-8 concentrations and GE in the peritoneal fluid were examined in 27 patients who underwent various types of elective abdominal surgery. We compared these results with clinical parameters of surgical stress, operating time (OT) and blood loss during the operation (BL). P-IL-6 and P-IL-8 were significantly correlated with OT (P-IL-6; r = 0.67, P < 0.001: P-IL-8; r = 0.59, P < 0.001) and BL (P-IL-6; r = 0.61, P < 0.001: P-IL-8: r = 0.48, P < 0.01). P-IL-8 was significantly correlated with P-IL-6 (r = 0.68, P < 0.001) and there was a positive correlation between GE and P-IL-8 (r = 0.37, P < 0.05). These findings indicate that IL-8 might activate granulocytes in the peritoneal cavity after elective abdominal surgery and that assaying P-IL-6 and P-IL-8 is useful in assessing the host's response to surgical stress.
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PMID:Peritoneal interleukin-6, interleukin-8 and granulocyte elastase activity after elective abdominal surgery. 783 3

Chronic airway inflammation is an important feature of cystic fibrosis (CF), markedly influencing morbidity and mortality. We wanted to assess the contribution of the respiratory epithelium in the mediation of local inflammatory events, and, more particularly, its regulating role through cytokine secretion. We have studied the regulation of interleukin-6 and 8 (IL-6 and IL-8) production by the SV40 transformed airway epithelial cell line JME/CF15 (homozygous for the deletion of Phe 508). We show that unstimulated JME/CF15 cells secrete IL-6 and IL-8. Neutrophil chemotactic activity (NCA) is detected in supernatants. The secretion of IL-6 and IL-8 is increased following stimulation of the JME/CF15 cells by IL-1 beta and neutrophil elastase. Lipopolysaccharide and granulocyte macrophage colony stimulating factor (GM-CSF) have no effect on secretion of IL-6 or IL-8. Neutrophil elastase inactivates recombinant human IL-6 at 37 degrees C in vitro, but has no effect at 4 degrees C, suggesting a proteolytic effect of elastase on IL-6. IL-8 activity remains preserved, even after prolonged exposure to elastase. Our data suggest that the airway epithelium may play an active role in the mediation of neutrophil chemotaxis. Local production of IL-8 in response to elastase and IL-1 beta, together with the inactivation of the anti-inflammatory protein IL-6, may result in a significant upregulation of airway inflammation in cystic fibrosis.
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PMID:Regulation of cytokine secretion by cystic fibrosis airway epithelial cells. 811 34

Chronic lung disease of prematurity (CLD) is a common respiratory disorder of preterm infants. At autopsy, fibroblast proliferation, and components of the extracellular matrix, including collagen and fibronectin, are markedly increased in the lungs of infants who die from CLD. Examination of broncho-alveolar fluid suggests that the persistence of neutrophils is associated with the development of CLD. In our studies, the pro-inflammatory cytokines, interleukin-1 beta (IL-1 beta) and interleukin-6, (IL-6) and mediators which reflect neutrophil recruitment and activation, including soluble intercellular adhesion molecule, interleukin-8 (IL-8) and neutrophil elastase, were increased in lavage fluid obtained from infants who developed CLD when compared to infants who did not. Furthermore, semiquantitative reverse transcriptase-polymerase chain reaction of mRNA extracted from lavage cells suggested that luminal cells may be the source of IL-6 detected in lavage fluid but non-luminal cells may be the sources of IL-1 beta and IL-8. Fibrosis is thought to be mediated by the pro-fibrotic cytokines including transforming growth factor-beta1 (TGF-beta 1). Both active and total TGF-beta 1 were increased in lavage fluid from infants who developed CLD. Furthermore, both type I procollagen and TGF-beta were increased qualitatively in lung tissue obtained at autopsy from infants who died from respiratory failure. The increase in inflammatory mediators was maximal at 10 days of age. By contrast, the increase in TGF-beta 1 was maximal at 4 days of age. This suggests that the interaction between inflammation and fibrosis in CLD is complex, and that prenatal factors may be important in the pathogenesis of CLD.
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PMID:Cytokines in chronic lung disease of prematurity. 883 40

Interleukin-6, interleukin-8, and polymorphonuclear leukocyte elastase levels in coronary sinus blood were measured and compared with those in arterial blood drawn from the radial artery before and immediately after cardiopulmonary bypass (CPB) during coronary artery bypass grafting in 20 patients. We introduced coronary sinus blood sampling as a useful method for evaluation of myocardial metabolism, myocardial protection, and reperfusion injury during CPB, especially by measurement of cytokines. Because interleukin-6, interleukin-8, and polymorphonuclear leukocyte elastase are inflammatory mediators, we speculated that they might show higher levels in coronary sinus blood than in systemic arterial blood. The results obtained from the 20 patients showed that levels of interleukin-6, interleukin-8, and polymorphonuclear leukocyte elastase increased immediately after CPB (p < .01), but there was no significant difference in these levels between coronary sinus and systemic arterial blood. We conclude that the myocardium is not a predominant source of their release during CPB. Our results also showed that the measurement of these cytokines in systemic arterial blood reflected their levels in the whole body, including the myocardium, even during cardiac operation with CPB.
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PMID:Measurement of cytokine levels by coronary sinus blood sampling during cardiac surgery with cardiopulmonary bypass. 894 90

Neutrophil activation is considered to play a major role in organ dysfunction after severe trauma. Major surgery like esophagectomy also induces various host responses including neutrophil activation and it may be responsible for postoperative complications. We measured neutrophil elastase releasing capacity in 14 patients undergoing esophagectomy to evaluate perioperative changes of neutrophil activation. Elastase releasing capacity was estimated by the fMLP-induced elastase release from separated neutrophils in vitro and expressed as % increase of released elastase activity induced by 0.2 microM fMLP. Elastase releasing capacity was significantly increased from 28.6 +/- 17.7% after induction of anesthesia to 63.7 +/- 38.8% at 72 hours after induction, and decreased to 57.6 +/- 15.4% at 72 hours after induction. Elastase alpha 1-antitripsin inhibitor complex showed no significant increase during perioperative period. Interleukin-6 showed a peak level 24 hours after induction and interleukin-8 was increased significantly 12 hours after induction and maintained the elevated level until 72 hours postoperatively. We concluded that the neutrophil activity was increased during the perioperative period of esophagectomy and the priming of neutrophil took place during extensive surgical intervention.
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PMID:[Evaluation of neutrophil activation using elastase releasing capacity in vitro during perioperative period of esophagectomy]. 902 81

Alpha-1 proteinase inhibitor (A1-Pi) is the main serine proteinase inhibitor found in human plasma and is a potent elastase inhibitor in various tissues, including lung. A1-Pi is expressed and induced in liver during inflammatory responses but can also be produced by epithelial cells. Since hepatocyte A1-Pi production is stimulated by interleukin-6 (IL-6) and other gp130-cytokines, such as leukemia inhibitory factor (LIF) and oncostatin M (OM), we investigated the role of these cytokines in regulating A1-Pi in lung epithelial cells. We show that OM, a monocyte and T cell product, can specifically and potently induce A1-Pi production in lung-derived A549 alveolar (epithelial) cells, as well as in liver-derived HepG2 cells. Both A1-Pi protein (as detected by ELISA and Western blots) and mRNA levels were enhanced 20-fold to 30-fold in A549 cells. OM was also able to stimulate the expression of tissue inhibitor of metalloproteinase-1 in these cells. Interestingly, other members of the IL-6 family (IL-6 and LIF) had little or no effect on A549 cells, and proinflammatory cytokines, such as IL-1 beta and tumor necrosis factor-alpha (TNF-alpha) also had no stimulatory effect on A1-Pi synthesis in A549 cells. Costimulation with IL-1 beta resulted in a decrease in A1-Pi production from OM-stimulated A549 cells. However, IL-6 production was synergistically enhanced. OM was also able to stimulate A1-Pi production from a bronchial epithelial primary cell line, whereas an intestinal epithelial cell line HT29 responded to IL-6 but not OM. These results suggest that lung levels A1-Pi could be derived not only from liver and inflammatory cells but also from epithelial cells, which can be upregulated on stimulation by OM. This may have implications for regulation of local activity of human neutrophil elastase (HNE) in such diseases as emphysema and cystic fibrosis.
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PMID:Oncostatin M, but not interleukin-6 or leukemia inhibitory factor, stimulates expression of alpha1-proteinase inhibitor in A549 human alveolar epithelial cells. 919 1

We measured circulating and sputum-sol concentrations of interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-alpha), neutrophil elastase-alpha1-antiproteinase complex (NEAPC), and C-reactive protein (CRP) in an exacerbation, after antibiotic treatment, and in clinically stable patients with cystic fibrosis and chronic pulmonary infection with Pseudomonas aeruginosa. The aim was to determine the compartmental patterns of a proinflammatory and anti-inflammatory cytokine compared with other markers of inflammatory activity in cystic fibrosis. IL-6, NEAPC, CRP, and absolute neutrophil count were reduced after antibiotic treatment, p < 0.01. IL-6 and CRP concentrations were greater, p = 0.007, and p = 0.01, respectively, in a stable group of patients compared with those at the end of an exacerbation. IL-6 and CRP concentrations were related (r = 0.836, p < 0.0001), and both were greater than in matched control subjects (p < 0.001) at all times studied. Sputum-sol concentrations of IL-6 after treatment were positively related to FEV1 and FVC and inversely related to concentrations of neutrophil elastase. The separation between patients and healthy subjects, and the reduction of IL-6 after antibiotic treatment indicates it could be used as a marker of inflammation, but its relationship to other markers depends on the compartment in which it is measured.
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PMID:Circulating immunoreactive interleukin-6 in cystic fibrosis. 962 Sep 3


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