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)

Patients with obstructive jaundice frequently suffer postoperative complications. We have investigated the relationship of obstructive jaundice to the neutrophil oxidase response and the "priming" of the response by the cytokines TNF alpha, interleukin-1 (IL-1), IL-6, and IL-8. On stimulation with f-met-leu-phe (fmlp), the respiratory burst in neutrophils from jaundiced patients was greatly increased compared with controls (p < 0.01), jaundiced patients having the highest respiratory burst levels were those with the poorest prognosis. Neutrophils from controls were primed by all the cytokines tested, whereas "jaundiced" cells were primed only by IL-1, and not by TNF alpha, IL-6, or IL-8, which in fact produced slight inhibition. We conclude that neutrophils from obstructive jaundiced patients have raised oxidative responses which may be due to "pre-priming" in vivo by cytokines, such as IL-6, IL-8, or TNF alpha. This exaggeration of the oxidative response in circulating neutrophils may contribute to the peri-operate complications of patients with obstructive jaundice.
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PMID:Neutrophil priming by cytokines in patients with obstructive jaundice. 820 47

The effect of n-6 fatty acids, particularly gamma-linolenic acid (GLA), on the oxidase response and neutrophil priming by tumour necrosis factor alpha and interleukin 8 was studied in both normal volunteers and patients with obstructive jaundice. GLA inhibited the neutrophil respiratory burst at concentrations higher than 50 mummol/l, but abolished cytokine priming at concentrations as low as 1 mummol/l. Inhibition was not the result of either cytotoxicity to the neutrophils or alteration in cytosolic free calcium homoeostasis. It is concluded that GLA is a potential inhibitor of neutrophil priming by cytokines and of the oxidative response.
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PMID:Inhibition of neutrophil respiratory burst and cytokine priming by gamma-linolenic acid. 911 34

Endotoxin contributes to cholangitis. We measured concentrations of bile and serum endotoxin and serum cytokines after biliary drainage for obstructive jaundice with or without acute cholangitis. Patients who underwent percutaneous transhepatic cholangiodrainage (PTCD) in 1995 were classified as having acute cholangitis (group A; n = 11), having a history of acute cholangitis (group B; n = 5), or not having a history of acute cholangitis (group C; n = 13). Bile endotoxin was positive (above the cut-off value) in all patients in groups A and B, and in five patients in group C. The mean concentration of bile endotoxin was significantly higher in groups A and B than in group C. After PTCD, the bile endotoxin level decreased more slowly in group A than in the other groups. Before PTCD, the mean serum levels of IL-1 receptor antagonist (IL-1ra), IL-6, and IL-8 were higher in group A than the other groups. The serum levels of IL-1ra and IL-6 before PTCD were significantly higher when the acute cholangitis was more severe. The mean serum levels of cytokines increased just after PTCD and then decreased. In group A, the serum level of IL-6 at 5 h after PTCD was significantly correlated to the endotoxin level in bile at this time. Increases in cytokines may participate in the pathophysiological changes of acute cholangitis. Biliary drainage for acute cholangitis causes improvement by decreasing the bile endotoxin level addition to decreasing bile-duct pressure, thereby preventing excess production of inflammatory cytokines.
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PMID:Concentrations of bile and serum endotoxin and serum cytokines after biliary drainage for acute cholangitis. 934 91

The effect of obstructive jaundice on neutrophil chemotactic function was investigated, with a potent chemotactic factor, IL-8 (recombinant rat GRO-beta), in rats that received 7-day bile duct ligation. Carrageenin or IL-8 was injected into a preformed air pouch, and exudate was collected 4 h later for measurement of myeloperoxidase activity. In vitro chemotaxis of peripheral neutrophils to IL-8 was evaluated by a modified Boyden chamber method. Both carrageenin and IL-8 induced significantly pronounced intra-air pouch neutrophil recruitment in the bile duct-ligated group compared with a sham-ligated group. In vitro neutrophil chemotaxis was significantly increased in the bile duct-ligated group compared with the sham-ligated group. The present experimental model suggests enhanced neutrophil chemotaxis to IL-8 in obstructive jaundice.
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PMID:Influence of biliary obstruction on neutrophil chemotaxis. 971 38

Excessive production of hydroxyl radicals in blood and liver has previously been demonstrated by us in rats with obstructive jaundice induced by common bile duct ligation (CBDL). In this study, we demonstrate overproduction of superoxide radicals in circulating blood of CBDL rats by the lucigenin-amplified chemiluminescence technique. To pinpoint the molecular agents that mediate these processes, we measured circulating proinflammatory cytokines, such as tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta ( IL-1beta), and interleukin-6 (IL-6) in controls and CBDL rats. Concentrations of these cytokines in blood of CBDL rats were markedly elevated when compared to the controls (TNF-alpha: 36.7 +/- 5.0 vs 13.8 +/- 0.5 pg/mL; IL-6: 2,814 +/- 1,740 vs 0 pg/mL; IL-1beta: 11.9 +/- 2.6 vs 0 pg/mL). The overproduction of free radicals triggered by elevated cytokines in CBDL rats was correlated with the activation of NF-kappaB in hepatic tissue. Using the TdT-mediated dUTP nick-end label staining technique, we showed that hepatic tissue sections from CBDL rats had an increase in the apoptotic index (AI). Based on these findings, we propose that the severe hepatic injury in CBDL rats is mediated by a cycle that involves the activation of NF-kappaB by combined action of proinflammatory cytokines and reactive oxygen species (ROS). NF-KB, in turn, initiates the transcription of cytokine genes (eg, IL-6, IL-8, TNF-alpha), which triggers hepatic injury, at least in part, by a free radical-mediated apoptotic mechanism. Elevated ROS may be as a positive-feedback signal that triggers NF-KB reactivation; the severe hepatic injury of CBDL rats may result from perpetuation of this vicious cycle.
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PMID:Free radical-triggered hepatic injury of experimental obstructive jaundice of rats involves overproduction of proinflammatory cytokines and enhanced activation of nuclear factor kappaB. 1168 50