Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P10145 (IL-8)
 23,849 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nitric oxide (NO.) can induce transient [Ca2+] changes in endothelial cells not different from receptor mediated signalling. Whether this Ca2+ signal may provide a link with IL-8 secretion induced by NO. donors was investigated in human endothelial cells. Sodium nitroprusside (SNP) and S-nitroso-N-acetyl-DL-penicillamine (SNAP) dose dependently increased IL-8 production in this cell type. Additive IL-8 secretion was found with TNFalpha. Buffering intracellular Ca2+ with MAPT/AM suppressed NO. induced [Ca2+]i changes and reduced subsequent IL-8 secretion. The additive effect of both NO. donors on TNFalpha induced IL-8 secretion was completely blocked in the presence of MAPT/AM. SKF 96365, which has been shown to block receptor mediated Ca2+ entry, and TMB-8, which blocks intracellular Ca2+ release, both inhibited IL-8 secretion, particularly when TNFalpha was used as a costimulator, indicating that [Ca2+]i changes are important components of IL-8 induction by NO..
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PMID:Intracellular Ca2+ dependence of nitric oxide mediated enhancement of interleukin-8 secretion in human endothelial cells. 935 Sep 89

The authors studied the relationship between cardiac cytokine release and pump function and whether low-dose application of sodium nitroprusside (SNP) improves cardiac performance during coronary artery bypass graft (CABG) creation. Cardiac reperfusion and application of nitric oxide have an influence on cytokine release. However, the functional consequences are unclear. Patients with CABGs (n = 30) with severely compromised left ventricular ejection fraction (<40%) were treated with either SNP (0.5 microg/kg/min) or placebo for the first 60 minutes of reperfusion after cardiac arrest. Interleukin (IL)-6, IL-8, and tumor necrosis factor (TNF)-alpha were determined in blood samples from the radial artery and coronary sinus during reperfusion (5, 35, and 75 minutes). Hemodynamic measurements were performed before and after cardiopulmonary bypass and at the end of surgery. In all patients, the cardiac index at the end of surgery correlated negatively with levels of TNF-alpha at 5 minutes (r = 0.398; P < 0.05), IL-8 at 35 minutes (r = 0.394; P < 0.05), and IL-6 at 75 minutes of reperfusion (r = 0.421; P < 0.025). Sodium nitroprusside improved the cardiac index immediately after reperfusion (4.4 L/min/m2 +/- 0.3 vs. 3.7 L/min/m2 +/- 0.1; P = 0.014) and at the end of surgery (3.8 L/min/m2 +/- 0.3 vs. 3.0 L/min/m2 +/- 0.2; P = 0.023). The negative correlation between cardiac index and transcardiac cytokines suggests that reducing cardiac inflammatory reaction improves postischemic cardiac function. This was achieved by treating CABG patients with the nitric oxide donor SNP at a dosage without vasodilatory action.
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PMID:Beneficial effect of sodium nitroprusside after coronary artery bypass surgery: pump function correlates inversely with cardiac release of proinflammatory cytokines. 1296 Jun 82

Nitric oxide (NO*) is a gaseous mediator synthesized by nitric oxide synthases. NO* is involved in the modulation of inflammation, but its role in airway inflammation remains controversial. We investigated the role of NO* in the synthesis of the chemokines interleukin-8 and monocyte chemotactic protein-1, and of intercellular adhesion molecule-1 by human airway epithelial cells. normal human bronchial epithelial cells and the bronchial epithelial cell line BEAS-2B were used. interleukin-8 (IL-8) and monocyte chemotactic protein-1 (MCP-1) secretion and intercellular adhesion molecule-1 (ICAM-1) expression were measured by ELISA. mRNA was assessed by semiquantitative RTI-PCR. Interleukin-8 secretion was significantly reduced after 24h incubation with the NO* donor, sodium nitroprusside. The effect was dose-dependent. Similar results were obtained with S-nitroso-N-D,L-penicillamine and S-nitroso-L-glutathione. Inhibition of endogenous NO* with the nitric oxide synthase inhibitor N-nitro-L-arginine-methyl-ester caused an increase in IL-8 secretion by lipopolysaccharide- and cytokine-stimulated BEAS-2B cells. Sodium nitroprusside also caused a reduction in monocyte chemotactic protein-1 secretion by both cell types. In contrast, intercellular adhesion molecule-1 expression was upregulated by sodium nitroprusside. RTI-PCR results indicate that the modulation of protein levels was paralleled by modification in mRNA levels. NO* has divergent effects on the synthesis of different inflammatory mediators in human bronchial epithelial cells.
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PMID:Divergent effects of nitric oxide on airway epithelial cell activation. 2152 74