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Query: UNIPROT:P10145 (IL-8)
 23,849 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Systemic Inflammatory Response Syndrome (SIRS) is a new concept of entry criteria for sepsis. This concept, when applied to area of Multiple Organ Failure (MOF), is considered to be a preparatory state for MOF. To study the significance of SIRS state at cardiac surgery, we measured the body temperature, white blood cell count, respiratory rate and heart rate of 18 patients who underwent elective cardiac surgery, from the 1st post-operative day to the 7th post-operative day. We also measured Interleukin-6 and 8 (IL-6 and IL-8) to understand the relationship between the SIRS state and inflammatory cytokines just after cardiopulmonary bypass (CPB), at the 1st, 3rd and 6th postoperative day. The result was as follows: Patients with CPB more than 120 minutes have more frequency and longer duration of SIRS than patients with CPB less than 120 minutes. Serum levels of IL-8 at SIRS state were revealed statistically higher than at non-SIRS case. Duration of SIRS state was related to CPB time and serum levels of IL-6 and IL-8 just after CPB. We concluded that SIRS state is an indication for anti-cytokine therapy to prevent MOF, and it is important to shorten CPB time in order to decrease the duration of SIRS.
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PMID:[Significance of systemic inflammatory response syndrome at cardiopulmonary bypass]. 875 88

TNF is produced by monocytes/macrophages in response to endotoxin, which may lead to septic shock. TNF stimulates neutrophil adherence, degranulation, and superoxide production, but inhibits neutrophil migration. A mitigating anti-inflammatory effect can be experimentally induced in septic shock by TNF blockers, such as pentoxifylline, and is also suggested for treatment with hrG-CSF. With regard to the combination of pentoxifylline and hrG-CSF, the purpose of this investigation was to explore whether and in what way the effects of hrG-CSF and pentoxifylline interact with each other in neutrophils. To this end, we studied the effects of pentoxifylline on TNF- and G-CSF-induced modulation of neutrophil chemotaxis and O2 release. TNF and G-CSF decreased directed migration of neutrophils to FMLP or IL-8. High-dose pentoxifylline (1 mM) was able to counteract the effect of TNF but not that of G-CSF on neutrophil migration. In the presence of pentoxifylline, TNF and G-CSF were unable to stimulate respiratory burst. In contrast, pre-exposure of cells to pentoxifylline followed by washing increased the priming effect of TNF or hrG-CSF on neutrophil respiratory burst activity. The methylxanthine derivative by itself showed no effect on spontaneous and fMLP-stimulated O2 release by neutrophils. Stimulation of neutrophil respiratory burst by pentoxifylline may not be detectable in the presence of pentoxifylline due to its known oxygen-radical scavenging function. Results suggest that by blocking the inflammatory action of TNF on neutrophils, pentoxifylline may diminish endothelial cell damage caused by inhibited neutrophil chemotaxis. On the other hand, since transiently present pentoxifylline may enhance the respiratory burst activity of TNF- or hrG-CSF-primed neutrophils, concomitant administration of pentoxifylline and hrG-CSF to patients with SIRS/sepsis might diminish beneficial effects of the latter and additional deleterious effects might occur.
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PMID:Pentoxifylline differentially regulates migration and respiratory burst activity of the neutrophil. 970 61

Inflammatory mediators include endotoxin (ETX), cytokines (interleukins [ILs], tumor necrosis factors [TNFs], and interferons), eicosanoids (prostaglandins and thromboxanes), reactive oxygen species (O2-, NO, and ONOO-), complements (C3 and C4), and stress hormones (catecholamine, cortisol, vasopressin, and growth hormone). These mediators work to maintain homeostasis under stressful conditions through a complex chain reaction or cascade that results in transient tissue damage known as the inflammatory response. The inflammatory response is decreased by a negative feedback system, which consists not only of the self-inhibitory action of ETX, TNF-alpha, IL-1, and IL-8, but also of the production of antiinflammatory mediators such as IL-4, -10, -11, and -13, TGF-beta, IL-Ra, and sTNFR. If excessive stress or a second attack of stress results in a higher level of inflammation-producing mediators than of inflammation-inhibiting mediators, tissue destruction occurs due to activation and infiltration of inflammatory cells or necrosis due to endothelial injury is seen, followed by disruption of homeostasis, organ dysfunction, and organ failure (multiple organ dysfunction syndrome [MODS] or multiple organ failure [MOF] induced by SIRS). In experimental liver dysfunction after 95% hepatectomy, massive apoptosis of hepatocytes is induced by prolonged hypercytokinemia, ONOO- production, decreased mitochondrial membrane potential of hepatocytes, and decreased Bc12 levels. On the other hand, if the antiinflammatory response is greater than the inflammatory response (CARS) a compromised state and refractory infection are seen, followed by progressive, irreversible organ dysfunction (MODS or MOF induced by CARS).
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PMID:[Inflammatory mediator and organ dysfunction syndrome]. 978 83

SIRS is a systemic inflammatory reaction occurring in the course of several diseases and it is considered that SIRS is hyper-cytokinemia. Recently, the control mechanism of IL-10 anti-inflammatory cytokine for the superfluous inflammatory reaction by inflammatory cytokines such as TNF has received considerable attention. IL-10 tends to inhibit monocytes/macrophages and the production of TNF, IL-1 and IL-8 is suppressed. In addition, the production of oxygen radicals and proteases from activated neutrophils is directly suppressed. IL-10 seems to control the generation of tissue injury that accompanies neutrophil activation by also suppressing CD11a, CD11b and TNF receptor expression of neutrophil surface directory. In this study, we observed the effect of a drug that controls cytokine production by lymphocytes after LPS loading, using an antibacterial agent and steroids, to observe the effect of the drug on the control mechanism of SIRS. As the result, TNF production by lymphocytes was suppressed by macrolide, new quinolone and fosphomycin. Steroid also dosage-dependently suppressed TNF production of lymphocytes after 24 hours of incubation while IL-10 production increased. From these results, it was considered that some antibacterial agents and steroids have anti-inflammatory or a modulating effect on inflammation. Clinically, the control of inflammation in patients with SIRS by these drugs is expected.
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PMID:[Modulation of SIRS]. 1089 69

We studied 174 patients with SIRS criteria, 45 with sepsis, eight with severe sepsis and 13 with septic shock. Serum TNF-alpha, IL-6, IL-8 and IL-10 levels were raised in SIRS patients, even in those cases in which an infection could not be documented, and more intensely in severe sepsis and in patients who died (11%). The slope of the regression line between IL-10 and TNF-alpha was sharper in patients with severe sepsis and in those who died; an imbalance between pro- and anti-inflammatory cytokines may be related to poor prognosis. Increased IL-6 and IL-10, decreased muscle mass, raised BUN and low body temperature were all independently related to prognosis.
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PMID:Prognostic value of cytokines in SIRS general medical patients. 1156 84

Biallelic polymorphism in the promotor region of the TNF-alpha gene have been associated with variation in TNF-alpha production. We determined the TNFA polymorphism (position--308) and related these data to plasma cytokine levels of TNF alpha, IL6, IL6R and IL8 in patients with SIRS and sepsis. Although there seems to be a different cytokine secretion pattern for both allelic groups (TNFA1 and TNFA2), a clear risk group could not be determined. It still remains unclear whether there is a genetic factor that influences the development of sepsis and multi organ failure.
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PMID:[Tumor necrosis factor-alpha (TNF-alpha) gene polymorphism in surgical intensive care patients with SIRS]. 1451 81

Microvascular endothelial cells (mECs) circulate at higher numbers in patients with severe sepsis and hemophagocytic syndromes. Although these blood mECs might stem from damaged microvasculature, they are perfectly viable and lead to the establishment of cell lines. Such mECs were cultured in low-dose human serum pools (0.5%) and MEM-alpha medium. Antigenic profiling revealed the expression of CD36, factor VIIIa, CD95-ligand, and CD44, but also CD146. We studied the antioxidative effect of the hematopoietic growth factor G-CSF(1) after in vitro stimulation with LPS from E. coli 0111:B4; the growth factor appeared to exhibit a protective effect on organ function in patients with SIRS. mECs were stimulated with 1 micro g/mL of LPS for 24 h and 48 h with and without G-CSF (3x10(3) U/mL) preincubation. After 24 h, supernatants of the stimulated mEC were tested for IL-8 by ELISA, and cells were tested for hemoxygenase-1 (HO-1, Hsp32) by immunohistochemistry and flow cytometry using OSA110 (mAb, Stressgene). Stimulation with LPS upregulated IL-8 by a factor of 2 to 10 in mEC. Preincubation with G-CSF markedly downregulated the LPS-induced IL-8 secretion (20-50%), but IL-6 production was not affected. Upon 48 h of LPS stimulation, mECs developed massive signs of apoptosis and concomitant caspase 3 activation. Caspase 3 activity induced by LPS (24 h) or by staurosporin (6 h) was found to be dramatically downregulated by the G-CSF preincubation protocol.
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PMID:G-CSF modulates LPS-induced apoptosis and IL-8 in human microvascular endothelial cells: involvement of calcium signaling. 1503 98

Severe sepsis and trauma complicated with multiple organ dysfunction syndrome (MODS) are among the leading causes of death in intensive therapy units, with mortality rate exceeding 50%. The outcome is not determined only by infection or trauma, but also by the intensity of immuno-inflammatory response, which is essential for host defence, but if uncontrolled leads to MODS. Pro-inflammatory cytokines (tumor necrosis factor-alpha--TNF-alpha, IL-1, IL-8, IL-12, IFN-gamma, etc.) represent a part of this immuno-inflammatory response to an insult. The results of the clinical investigation of correlation between pro-inflammatory cytokines (IL-8, IL-12, TNF-alpha, IFN-gamma), the outcome (survivors, non-survivors), and the severity (systemic inflammatory response syndrome--SIRS--less severe, and MODS--more severe) in polytraumatised patients with sepsis are presented in this paper. Mean values of IL-8 were 1.3-fold higher in non-survivors (p<0.05), and 60-fold higher in MODS group (p<0.01). Mean values of IL-12 were 1.6-fold higher in survivors (p<0.01), while the values between SIRS and MODS group did not differ significantly; mean values of TNF-alpha were 3-fold higher in survivors (p<0.05), and 46-fold higher in MODS group (p<0.01). Mean values of IFN-gamma did not differ significantly between the two groups regarding the outcome and severity. The obtained results indicated that IL-8 was a reliable predictor of lethal outcome and MODS (p<0.01), IL-12 a reliable predictor of survival (p<0.05), and TNF-alpha a reliable predictor of survival (p<0.05) and MODS (p<0.01).
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PMID:[Importance of determination of proinflammatory cytokines in the blood of polytraumatized patients with sepsis]. 1529 18

Bacterial factors stimulate the release of tissue factor as well as proinflammatory and antiinflammatory cytokines. TNF augments inflammation, TNF and IFN-gamma induce coagulation, and IL-1beta induces coagulation and fibrinolysis. IL-8 augments synergistic inflammation and coagulation. IL-6 augments coagulation and inhibits fibrinolysis. IL-10 inhibits inflammatory process and inhibits fibrinolysis. IL-4, IL-13, and TGF-beta act for anticoagulation. Administration of IL-2, G-CSF or IFN-gamma has been reported to have side effect of induction of coagulation. IL-12 induces coagulation first and fibrinolysis later. On the other, tissue factor induces proinflammatory (except TNF) and antiinflammatory cytokines, and thrombin enhances inflammation. Patients who died of SIRS/sepsis have been complicated with hypercoagulopathy and impaired fibrinolysis correlated with increased IL-10 production. Inhibition of IL-10 production or administration of fiblynolitic agents may be useful. Recently, activated protein C (APC) which has antiinflammatory effect has been paid attention in the treatment of SIRS/sepsis.
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PMID:[Correlation between intravascular coagulation/fibrinolysis system and cytokines]. 1559 92

Severe trauma induces sustained changes of the immune response, which are thought to be related to secondary organ dysfunction. Despite a similar injury severity, the extent of the inflammatory response may vary between polytraumatized patients. It is unclear whether inflammatory variability is associated with genetic variations. In this prospective cohort study, patients were included when the following criteria were fulfilled: Injury Severity Score >16, age 18 to 60 years, and a survival >48 h after injury. Four different polymorphisms (TNF-Nco1, IL-1-Taq1, IL-6-174G/C, and IL-8-251A/T) were determined. Patients were separated according to the severity of the systemic inflammatory response syndrome (SIRS; ACCP/SCCM criteria: >2 criteria at 2 consecutive days or at 3 days of the observation period: group +SIRS; <or=2 criteria: group -SIRS). Ninety-seven severely injured patients were included (-SIRS, 56 patients; +SIRS, 41 patients). A significantly higher incidence of the IL-6-174G allele and the IL-6-174G homozygous genotype in +SIRS patients was observed. The IL-6-174G/C polymorphism was associated with the severity of posttraumatic SIRS. This data points toward a genetic predisposition regarding an enhanced inflammatory response after polytrauma that may be associated with adverse outcome.
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PMID:Genetic predisposition for a compromised immune system after multiple trauma. 1631 81


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