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)

Recent studies have shown that opioid peptides are released from cells of the immune system during inflammation and stress, and are associated with altered immune responses. Moreover, concentrations of opioid peptides are increased in peripheral blood and at the sites of inflammatory reactions. The aim of this study was to evaluate immunological effects of opioid peptides endomorphins 1 and 2 on constitutive apoptosis, superoxide anion production, hydrogen peroxide production, adhesion, phagocytosis, and chemotaxis of neutrophils. Neutrophils were isolated by peritoneal lavage from rats. Endomorphins 1 and 2 significantly delayed constitutive neutrophil apoptosis. The delay of neutrophil apoptosis was markedly attenuated by LY294002, a phosphoinositide 3-kinase inhibitor. Moreover, endomorphins 1 and 2 activated the phosphoinositide 3-kinase pathway as determined by phosphorylation of BAD. In contrast, endomorphins 1 and 2 blocked the production of superoxide anion and hydrogen peroxide by PMA-stimulated neutrophils. In addition, endomorphins 1 and 2 inhibited neutrophil adhesion to fibronectin. Moreover, endomorphins 1 and 2 potentiated neutrophil chemotaxis toward zymosan-activated serum and IL-8, respectively. However, endomorphins 1 and 2 did not alter phagocytosis of Escherichia coli by neutrophils. These results suggest that endomorphins 1 and 2 may act to delay neutrophil apoptosis and alter the natural immune functions of neutrophils.
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PMID:Endomorphins delay constitutive apoptosis and alter the innate host defense functions of neutrophils. 1184 43

We previously reported that the fungal particle 1,3-beta-D-glucan derived from Candida albicans, a pathogenic fungus, was obtained by oxidation of the cell wall with sodium hypochlorite (NaClO). It could be solubilized by treatment with dimethylsulfoxide (DMSO). In the present study, we prepared Candida 1,3-beta-D-glucan having different physical properties, and examined the relationship between leukocyte activation and the physicochemical properties. Beta-glucan activated leukocytes significantly more effectively in a particulate than solubilized form in terms of TNF-alpha production by RAW 264.7 cells, hydrogen peroxide production by murine PEC and IL-8 production by human PBMC. Furthermore, we compared the biological activity of the glucan particles oxidized under various conditions. Interestingly, inactive and antagonistic particles were obtained under strong oxidation conditions. However, the inactive particles showed significant agonistic activity on dissolution in DMSO and following lyophilization. These facts strongly suggested that the solubility and assembly of the components influence the immunopharmacological activities of 1,3-beta-D-glucans.
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PMID:Relationship between the physical properties of Candida albicans cell well beta-glucan and activation of leukocytes in vitro. 1234 48

The 20 aminoacyl-tRNA synthetases catalyze the first step of protein synthesis and establish the rules of the genetic code through aminoacylation reactions. Biological fragments of two human enzymes, tyrosyl-tRNA synthetase (TyrRS) and tryptophanyl-tRNA synthetase, connect protein synthesis to cell-signaling pathways including angiogenesis. Alternative splicing or proteolysis produces these fragments. The proangiogenic N-terminal fragment mini-TyrRS has IL-8-like cytokine activity that, like other CXC cytokines, depends on a Glu-Leu-Arg motif. Point mutations in this motif abolish cytokine activity. The full-length native TyrRS lacks cytokine activity. No structure has been available for any mammalian tRNA synthetase that, in turn, might give insight into why mini-TyrRS and not TyrRS has cytokine activities. Here, the structure of human mini-TyrRS, which contains both the catalytic and the anticodon recognition domain, is reported to a resolution of 1.18 A. The critical Glu-Leu-Arg motif is located on an internal alpha-helix of the catalytic domain, where the guanidino side chain of R is part of a hydrogen-bonding network tethering the anticodon-recognition domain back to the catalytic site. Whereas the catalytic domains of the human and bacterial enzymes superimpose, the spatial disposition of the anticodon recognition domain relative to the catalytic domain is unique in mini-TyrRS relative to the bacterial orthologs. This unique orientation of the anticodon-recognition domain can explain why the fragment mini-TyrRS, and not full-length native TyrRS, is active in cytokine-signaling pathways.
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PMID:Crystal structure of a human aminoacyl-tRNA synthetase cytokine. 1242 73

Reactive oxygen species (ROS) have been counted among the potential toxic factors involving Helicobacter pylori (H. pylori)-induced gastric injury. Transcription nuclear factor-kappaB (NF-kappaB) is activated by ROS and regulates inflammatory gene expression. Thiol compounds, such as glutathione and N-acetylcysteine, scavenge hydrogen peroxide and are reported to prevent oxidative damage in various cells. The present study aims to investigate whether thiol compounds could affect H. pylori-induced IL-8 production by regulating transcription factor NF-kappaB in human gastric epithelial AGS cells. AGS cells were incubated with H. pylori (NCTC 11637) at a ratio of 1:100 in the presence or absence of thiol compounds. ROS generation was determined by confocal microscopy using ROS-sensitive dichlorofluorescein diacetate dye. Levels of hydrogen peroxide and IL-8 in the medium and DNA binding activity of NF-kappaB were determined by enzyme-linked immunosorbent assay, colorimetric assay, and electrophoretic mobility shift assay. Results indicated both thiol compounds inhibited H. pylori-induced hydrogen peroxide production, in accordance with their inhibition on NF-kappaB activation and IL-8 production induced by H. pylori in AGS cells. In conclusion, ROS may be a signaling molecule triggering NF-kappaB activation and the expression of inflammatory genes such as IL-8.
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PMID:Transcriptional regulation by thiol compounds in Helicobacter pylori-induced interleukin-8 production in human gastric epithelial cells. 1248 25

Acetylation of histone residues regulates the expression of inflammatory genes and is controlled by the activities of histone acetyltransferases (HAT) and histone deacetylases (HDAC). Analysis of histone acetylation in human cells is limited by the large numbers needed to perform activity assays or Western blotting. We have used flow cytometry to investigate changes in HAT and HDAC activities at the single cell level and to investigate the effect of hydrogen peroxide (H(2)O(2)) on histone H4 acetylation and cell-cycle progression. Using an anti-acetylated histone H4 antibody we show that H(2)O(2) induced a time-dependent increase in histone acetylation that was maintained for 12h. This was associated with increased IL-8 production. H(2)O(2) also affected cell-cycle progression. HAT activity was found to be highest in G2/M and equivalent in G0/G1 and S phases of the cell cycle. These data show that detection of acetylated histone residues at the single cell level using FACs may be a powerful new tool for the analysis of modulation of cell proliferation and gene transcription.
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PMID:The effect of oxidative stress on histone acetylation and IL-8 release. 1256 1

High PCO(2) levels attenuate reperfusion injury and ventilation-induced injury in isolated and perfused lungs. We asked whether premature lambs could tolerate 6 h of ventilation with a PCO(2) >80 mm Hg and whether the high PCO(2) modulated the ventilator-induced injury. Preterm surfactant-treated lambs were ventilated for 30 min with a high tidal volume (V(T)) to induce lung injury. The lambs then were ventilated for 5.5 h with a V(T) of 6-9 mL/kg to achieve a PCO(2) of 40-50 mm Hg in the control group. CO(2) was added to the ventilator circuit of a high PCO(2) group to maintain an average PCO(2) of 95 +/- 5 mm Hg. The high PCO(2) lambs had heart rates, blood pressures, plasma cortisol values, and oxygenation equivalent to the control lambs. The lungs of the high PCO(2) group had significantly higher gas volumes and had less lung injury by histopathology. Indicators of inflammation (white blood cells, hydrogen peroxide production, and IL-1beta and IL-8 cytokine mRNA expression in cells from the alveolar wash) qualitatively indicated less injury in the high PCO(2) group, although the differences were not significant. Preterm lambs tolerated a very high PCO(2) without physiologic compromise for 6 h. The high PCO(2) may attenuate ventilator-induced lung injury in the preterm.
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PMID:Effects of high PCO2 on ventilated preterm lamb lungs. 1259 96

Oxidants and inflammatory mediators such as tumour necrosis factor-alpha (TNF-alpha) activate transcription factors such as NF-kappa B. Interleukin-8 (IL-8) is a ubiquitous inflammatory chemokine that mediates a multitude of inflammatory events in the lung. Ergothioneine is a naturally occurring thiol compound, which possesses antioxidant property. The aim of this study was to determine whether ergothioneine can inhibit the hydrogen peroxide (H(2)O(2))- and TNF-alpha-mediated activation of NF-kappa B and the release of IL-8 in human alveolar epithelial cells (A549). Treatment of A549 cells with H(2)O(2) (100 microM) and TNF-alpha (10 ng/ml) significantly increased NF-kappa B activation using a reporter assay. Ergothioneine inhibited both H(2)O(2)- and TNF-alpha-mediated activation of NF-kappa B. Both H(2)O(2) and TNF-alpha significantly increased IL-8 release, which was inhibited by pre-treatment of A549 cells with ergothioneine compared to the control untreated cells. Ergothioneine also abolished the transcriptional activation of IL-8 in an IL-8-chloramphenicol acetyltransferase (CAT) reporter system, transfected into A549 cells. This indicates a molecular mechanism for the anti-inflammatory effects of ergothioneine.
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PMID:Ergothioneine inhibits oxidative stress- and TNF-alpha-induced NF-kappa B activation and interleukin-8 release in alveolar epithelial cells. 1264 50

The effects of grepafloxacin on the release of cytokines, chemical mediators, hydrolytic enzyme activities, and lipoxygenation in zymogen A- or Staphylococcus aureus-stimulated human THP-1 monocytes were evaluated. Initially, consistent with stimulation of phagocytic mechanisms of the monocytes, increases in cyclic adenosine monophosphate (cAMP) release, nitric oxide [NO] release, and hydrogen peroxide [H(2)O(2)] release, with a small decrease in cellular pH, occurred within 2 h. Enzymatic activities associated with oxygen burst of phagocytic cells (e.g., protein kinase C and nicotinamide adenine dinucleotide phosphate, reduced (NADPH) oxidase) were elevated, suggesting that monocytes attempted to destroy the invading organism through an innate phagocytic cidal immunologic mechanism. After 1-2 h of exposure to grepafloxacin, the oxygen burst and the release of proinflammatory cytokines and chemical mediators were suppressed. After 4 h, suppression of n-acetyl glucosaminidase (NAG) and cathepsin D activities and lipid peroxidation occurred, suppressing the pathogen-induced spread of infection and inflammation. Release of tumor necrosis factor (TNFalpha), interleukin (IL)-1, IL-6, and IL-8 was inhibited by grepafloxacin in a concentration-dependent manner, suggesting a reduction in the acute-phase inflammatory responses initiated by cytokine release from monocytes. Later, S. aureus were killed through inhibition of DNA synthesis, consistent with a bacteriostatic effect. Drug action against invading organisms appears to occur through multiple processes. Modulation of the innate immune system occurs within the first hour, causing the activation of cytokines, chemical mediators, and hydrolytic enzymes. A second phase between 2-4 h appears to involve the suppression of cellular components involved in inflammation and the spread of the infection. The third response, an apparent bacteriostatic inhibition of DNA synthesis, causes bacterial death.
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PMID:In-vitro anti-inflammatory and immunomodulatory effects of grepafloxacin in zymogen A- or Staphylococcus aureus-stimulated human THP-1 monocytes. 1282 12

Oxidative stress, IL-1alpha, and IL-8 are known to contribute to mucosal inflammation of the gastrointestinal tract. We examined the IL-8 response after brief exposure to hydrogen peroxide induced oxidative stress in CaCo-2 cells (a human colon carcinoma cell line) and in human intestinal epithelial cells. In addition, we examined whether exposure to oxidative stress, followed by IL-1alpha, could modulate IL-8 production. A transient up-regulation of IL-8 mRNA expression was observed after hydrogen peroxide treatment. Hydrogen peroxide induced oxidative stress was also observed to promote IL-8 secretion. Exposure to hydrogen peroxide, followed by IL-1alpha, enhanced IL-8 production over that achieved with IL-1alpha alone. Thus, oxidative stress and IL-1alpha were observed to cooperatively enhance IL-8 production.
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PMID:Combined effect of hydrogen peroxide induced oxidative stress and IL-1 alpha on IL-8 production in CaCo-2 cells (a human colon carcinoma cell line) and normal intestinal epithelial cells. 1287 65

We have examined the effects of various antioxidants and inhibitors of redox-sensitive signal transduction pathways on induction of interleukin 8 (IL-8) gene by NO in monocytic U937 cells. We have observed that nitrosoglutathione or another NO-generating compound spermine NONOate caused significant accumulation of IL-8 mRNA. Pretreatment of cells with pyrrolidine dithiocarbamate or with antioxidants, which scavenge hydroxyl radical, dimethyl sulfoxide (DMSO), or dimetylthiourea (DMTU) completely abrogated NO-dependent induction of IL-8 gene expression. The transcriptional activation of IL-8 gene was not affected by sodium formate or sodium salicylate, suggesting that suppression of the IL-8 gene induction is specific to the class of hydroxyl radical scavenger used. Furthermore, we have shown that IL-8 induction was not inhibited by catalase and the iron chelator deferoxamine, indicating that the inhibitory actions of DMSO and DMTU are not related to scavenging of reactive oxygen species produced from hydrogen peroxide in the iron-catalyzed reactions. Finally, we have not observed any significant inhibition of NO-dependent IL-8 gene induction by superoxide scavengers such as N-acetyl cysteine, uric acid, and superoxide dismutase. Therefore, it seems likely that in U937 cells, hydroxyl radicals or species with reactivity similar to hydroxyl radicals contribute to NO-mediated IL-8 gene induction.
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PMID:Redox modulation of NO-dependent induction of interleukin 8 gene in monocytic U937 cells. 1290 50


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