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)

The epidermal response to 2 different irritants, nonanoic acid (NAA) and sodium lauryl sulfate (SLS), was investigated with 2 different methods. NAA 80% and SLS 4% were applied under occlusion for up to 24 h. Elemental changes were determined in cryosections by x-ray microanalysis. Compared to unexposed skin a significantly higher sodium/potassium ratio was found after 6 h in NAA-exposed skin and a lower ratio in SLS-exposed. At 24 h both substances had induced similar changes, compatible with a cell injury. The findings demonstrate a time-dependent NAA and SLS response. With reverse transcription polymerase chain reaction, the mRNA expression of interleukin-1 alpha (IL-1 alpha), -1 beta (IL-1 beta), -6 (IL-6), and -8 (IL-8), tumor necrosis factor alpha (TNF alpha) and granulocyte macrophage colony stimulating factor (GM-CSF) in shave biopsies from irritated and unexposed skin was studied at 0. 4. 8 and 24 h. NAA, but not SLS, induced an increase in mRNA expression for IL-6 mRNA-expression for GM-CSF was increased after SLS exposure, but not after NAA. These findings indicate a time and substance dependent difference in the up-regulation of mRNA for different cytokines in epidermis during the first 24 h of the irritant reaction. This might be the effect of differences in the irritants action on the cell membranes, which is also reflected by the differences found in the elemental content at 6 h.
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PMID:Different pathways in irritant contact eczema? Early differences in the epidermal elemental content and expression of cytokines after application of 2 different irritants. 911 30

Interleukin (IL) 8 was measured in CSF of 14 patients with severe traumatic brain injury. IL-8 levels were significantly higher in CSF (up to 8,000 pg/ml) than serum (up to 2,400 pg/ml) (p < 0.05), suggesting intrathecal production. Maximal IL-8 values in CSF correlated with a severe dysfunction of the blood-brain barrier. Nerve growth factor (NGF) was detected in CSF of 7 of 14 patients (range of maximal NGF: 62-12,130 pg/ml). IL-8 concentrations were significantly higher in these patients than in those without NGF (p < 0.01). CSF containing high IL-8 (3,800-7,900 pg/ml) induced greater NGF production in cultured astrocytes (202-434 pg/ml) than samples with low IL-8 (600-1,000 pg/ml), which showed a smaller NGF increase (0-165 pg/ml). Anti-IL-8 antibodies strongly reduced (52-100%) the release of NGF in the group of high IL-8, whereas in the group with low IL-8, this effect was lower (0-52%). The inability of anti-IL-8 antibodies to inhibit the synthesis of NGF completely may depend on cytokines like tumor necrosis factor alpha and IL-6 found in these CSF samples, which may act in association with IL-8. Thus, IL-8 may represent a pivotal cytokine in the pathology of brain injury.
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PMID:Interleukin-8 released into the cerebrospinal fluid after brain injury is associated with blood-brain barrier dysfunction and nerve growth factor production. 911 1

The bone-cement interface tissue of failed total hip arthroplasty (THA) has inflammatory characteristics, such as the presence of prostaglandin E2 and interleukin 1 (IL-1). We considered that the bone-cement interface tissue could be the site of granulomatous inflammation caused by a foreign-body reaction. It has been demonstrated that inflammatory cytokines and chemokines have an important role in granulomatous inflammation. Bone-cement interface tissue was obtained at revision from nine patients with failed cemented THA, and the role of macrophages was assessed by immunohistochemistry, electron microscopy, and molecular biological techniques. We used the reverse-transcriptional polymerase chain reaction to examine the expression of mRNA for IL-1 alpha, IL-1 beta, tumor necrosis factor alpha (TNF alpha), macrophage inflammatory protein (MIP)-1 alpha, MIP-1 beta, IL-8, and monocyte chemoattractant protein. Polyethylene debris surrounded by macrophages and phagocytosis of debris by macrophages was frequently observed in the interface tissue. Macrophage activation and the production of inflammatory cytokines such as IL-1 and TNF alpha might induce the development of interface tissue. Expression of chemokine mRNAs was also commonly seen, suggesting that this led to recruitment of macrophages into the bone-cement interface tissue. Debris released from implants appears to cause activation of macrophages and the production of inflammatory cytokines and chemokines that induce cellular recruitment into interface tissue. This mechanism might form a vicious cycle that aggravates THA loosening.
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PMID:Macrophage activation and migration in interface tissue around loosening total hip arthroplasty components. 913 74

Polymorphonuclear leukocytes (PMN) are the first cells that migrate into periodontal tissues and gingival crevices in response to invading pathogens. It was recently demonstrated that PMN have the ability to synthesize and release cytokines following appropriate stimulation, while it is not clear whether these capacities are directly related to periodontal destructive processes. We therefore investigated the amounts of the cytokines interleukin-1 beta (IL-1 beta), tumor necrosis factor alpha (TNF-alpha), IL-8 and IL-1 receptor antagonist (IL-1ra) secreted by PMN from healthy donors following stimulation with lipopolysaccharide (LPS) from 4 periodontopathic bacteria, Porphyromonas gingivalis, Actinobacillus actinomycetemcomitans, Capnocytophaga ochracea and Fusobacterium nucleatum, and the non-oral bacterium Escherichia coli. A actinomycetemcomitans, F. nucleatum and E. coli LPS stimulated the release of significantly greater amounts of IL-1 beta, TNF-alpha and IL-8 than the control unstimulated PMN (p < 0.01). The levels of IL-1 beta, TNF-alpha and IL-8 released from cells stimulated with P. gingivalis or C. ochracea LPS were significantly lower than those of cells stimulated with A. actinomycetemcomitans or E. coli LPS (p < 0.05). On the other hand, substantially greater amounts of IL-1ra were released from PMN stimulated with each LPS and from control unstimulated PMN during the first 6 h, and then significantly greater amounts of IL-1ra were secreted by PMN stimulated with A. actinomycetemcomitans and E.coli LPS during the following 12 h (p < 0.01). The inhibitory effects of IL-1ra on the biological activity of IL-1 in the supernatants of PMN were examined by the thymocyte comitogen proliferation assay. The supernatants of PMN stimulated with each LPS showed less biological IL-1 activity as compared with the same doses of recombinant human IL-1 beta detected by enzyme-linked immunosorbent assay. Furthermore, no activity was detected in the supernatants of PMN stimulated with P. gingivalis or C. ochracea LPS. These findings demonstrated that LPS from periodontopathic bacteria were capable of stimulating PMN to release not only pro-inflammatory cytokines but also their inhibitors such as IL-1ra. Different secretion levels of these cytokines and their biological activities induced by the various LPS might be important in the onset and progression of periodontal diseases.
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PMID:Secretion of IL-1 beta, TNF-alpha, IL-8 and IL-1ra by human polymorphonuclear leukocytes in response to lipopolysaccharides from periodontopathic bacteria. 913 93

Inflammation is mediated by a variety of soluble factors, including a group of secreted polypeptides known as cytokines. Inflammatory cytokines can be divided into two groups: those involved in acute inflammation and those responsible for chronic inflammation. This review describes the role played in acute inflammation by IL-1, TNF-alpha, IL-6, IL-11, IL-8 and other chemokines, G-CSF, and GM-CSF. It also describes the involvement of cytokines in chronic inflammation. This latter group can be subdivided into cytokines mediating humoral responses such as IL-4, IL-5, IL-6, IL-7, and IL-13, and those mediating cellular responses such as IL-1, IL-2, IL-3, IL-4, IL-7, IL-9, IL-10, IL-12, interferons, transforming growth factor-beta, and tumor necrosis factor alpha and beta. Some cytokines, such as IL-1, significantly contribute to both acute and chronic inflammation. This review also summarizes features of the cell-surface receptors that mediate the inflammatory effects of the described cytokines.
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PMID:Cytokines in acute and chronic inflammation. 915 5

The gram-positive bacterium Streptococcus pyogenes (group A streptococcus) is the causative agent of a wide variety of suppurative infections of cutaneous tissues. Previous analyses have demonstrated that the M protein of S. pyogenes is an adhesin that directs the attachment of the streptococcus to keratinocytes in the skin. In this study, we have examined keratinocyte function in response to S. pyogenes and found that adherent versus nonadherent streptococci promote distinct patterns of expression of several proinflammatory molecules and keratinocyte cell fate. When analyzed by a quantitative reverse transcriptase PCR method, infection of cultured HaCaT keratinocytes with adherent, but not nonadherent, streptococci resulted in increased expression of mRNA for the cytokines interleukin-1alpha (IL-1alpha), IL-1beta, and IL-8 but neither infection induced expression of tumor necrosis factor alpha. In contrast, both adherent and nonadherent S. pyogenes induced expression of IL-6 and each promoted synthesis and release of prostaglandin E2 (PGE2). However, considerably greater levels of IL-6 expression were stimulated by adherent streptococci relative to nonadherent streptococci and the kinetics of PGE2 release in response to nonadherent streptococci was delayed compared to the response to adherent streptococci. Staining with the fluorescent probe ethidium homodimer-1 revealed that keratinocyte membranes were rapidly damaged upon infection with adherent streptococci but were not damaged by nonadherent streptococci. Finally, treatments which inhibited streptococcal metabolism completely blocked the ability of adherent streptococci to elicit responses. These data suggest that expression of an adhesin is a strategy used by S. pyogenes to modulate keratinocyte responses during infection of the skin and implicate additional streptococcal products in these signaling interactions.
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PMID:Keratinocyte proinflammatory responses to adherent and nonadherent group A streptococci. 916 41

We investigated whether a diet of increased carbohydrate content reduces the symptoms of acute mountain sickness (AMS) and whether concentrations of circulating cytokines rise and correlate with hypoxia and AMS. There were 19 healthy volunteers who ingested in randomized order both a high carbohydrate (68% CHO) or normal carbohydrate (45% CHO) diet for 4 d. On the 4th d, subjects were exposed to 8 h of 10% normobaric oxygen. Each subject completed the Lake Louise Consensus Questionnaire (LLCQ: a questionnaire developed to quantify the common symptoms and consequences of AMS) at the beginning and end of each hypoxic session, at which times venous blood was obtained for the following cytokines: interleukins 1 beta, 6 and 8 (IL-1 beta, IL-6, IL-8) and tumor necrosis factor alpha (TNF-alpha). AMS symptoms did not differ significantly between the diets (LLCQ scores: 68% CHO = 10.1 +/- 3.8 vs. 45% CHO = 10.3 +/- 4.1). Cytokine concentrations did not change with hypoxia on either diet, nor did individual changes correlate with AMS symptoms. We conclude that a high carbohydrate diet for 4 d does not reduce the symptoms of AMS; and plasma cytokine concentrations do not change with hypoxia and the development of AMS and, thus, are not likely mediators of this syndrome.
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PMID:Acute mountain sickness is not altered by a high carbohydrate diet nor associated with elevated circulating cytokines. 918 37

Ehrlichia chaffeensis is an obligatory intracellular bacterium that infects monocytes and macrophages and is the etiologic agent of human ehrlichiosis in the United States. Our previous studies showed that the exposure of human monocytes to E. chaffeensis induces the expression of interleukin-1beta (IL-1beta), IL-8, and IL-10 genes in vitro but not the expression of tumor necrosis factor alpha (TNF-alpha) and IL-6 mRNAs. In this study, the effect of anti-E. chaffeensis antibody complexed with E. chaffeensis on the expression of major proinflammatory cytokines in human monocytes was examined. Human monocytic cell line THP-1 was treated with E. chaffeensis which had been preincubated with human anti-E. chaffeensis serum for 2 h, and the levels of cytokine mRNAs were evaluated by competitive reverse transcription-PCR. Anti-E. chaffeensis antibody complexed with E. chaffeensis significantly enhanced mRNA expression of IL-1beta in THP-1 cells. The expression of TNF-alpha and IL-6 mRNAs was also induced. The levels of secreted IL-1beta, TNF-alpha, and IL-6 during 24 h of stimulation were comparable to those induced by Escherichia coli lipopolysaccharide at 1 microg/ml. Fab fragment of anti-E. chaffeensis immunoglobulin G complexed with E. chaffeensis did not induce any of these three cytokines, indicating that ehrlichial binding is required for IL-1beta mRNA expression and that binding of the immune complex to the Fc gamma receptor is required for TNF-alpha and IL-6 mRNA expression and enhanced IL-1beta mRNA expression. Furthermore, prolonged degradation of IkappaB-alpha and activation of NF-kappaB were demonstrated in THP-1 cells exposed to anti-E. chaffeensis serum and E. chaffeensis. This result implies that development of anti-E. chaffeensis antibody in patients can result in the production of major proinflammatory cytokines, which may play an important role in the pathophysiology of ehrlichiosis and immune responses to it.
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PMID:Anti-Ehrlichia chaffeensis antibody complexed with E. chaffeensis induces potent proinflammatory cytokine mRNA expression in human monocytes through sustained reduction of IkappaB-alpha and activation of NF-kappaB. 919 64

Interleukin (IL)-8 is a chemotactic cytokine that has been implicated in the etiology of infection-induced and normal human labor. In particular, IL-8 has been implicated in the processes of cervical ripening and rupture of fetal membranes because of its role in neutrophil activation and release of cellular matrix remodeling enzymes. In this study, we tested the hypotheses that IL-8 is released locally in the intrauterine environment from human amnion, choriodecidua, and placenta, and that IL-8 release from these tissues is increased by bacterial endotoxin, lipopolysaccharides (LPS), and inflammatory cytokines. IL-8 was released from human amnion, choriodecidual, and placental explants, with choriodecidua demonstrating the most abundant release. IL-8 release was significantly (multiple analysis of variance, p < 0.05) increased by LPS in a time- and dose-dependent manner from both choriodecidual and placental explants, but not from amnion explants. In addition, IL-1alpha (0.28 nM) and tumor necrosis factor alpha (TNFalpha, 10 nM) significantly (Student's t-test, p < 0.05) increased IL-8 release from placental explants 2- to 3-fold. These studies establish that the amnion, choriodecidua, and placenta are a source of IL-8 and demonstrate tissue-specific and differential regulation of IL-8 release by LPS, IL-1alpha, and TNF-alpha. These data support a role for IL-8 in a cascade of inflammatory events initiated by an intrauterine infection and resulting in activation of the labor process.
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PMID:Interleukin-8 release from human gestational tissue explants: the effects of lipopolysaccharide and cytokines. 928 99

We have demonstrated recently that methotrexate (MTX) inhibits superoxide generation and chemotaxis induced by N-formylmethionyl-leucyl-phenylalanine (fMLP) in neutrophils primed by granulocyte colony-stimulating factor (G-CSF). To extend these observations, we examined the in vitro effect of MTX on fMLP-stimulated superoxide generation and chemotaxis in neutrophils primed by either tumor necrosis factor alpha (TNF-alpha) or bacterial lipopolysaccharide (LPS). MTX inhibited superoxide generation and chemotaxis more efficiently in TNF-alpha- or LPS-primed neutrophils than in unprimed neutrophils. When either hypoxanthine or guanosine was added to the culture medium, the effects of MTX were partially counteracted. Furthermore, MTX caused a significant inhibition of both superoxide production induced by phorbol 12-myristate-13-acetate and chemotaxis induced by interleukin 8 in G-CSF-primed neutrophils. These results may support the hypothesis that neutrophils primed by different stimuli are more susceptible to the inhibitory effects of MTX on superoxide generation and chemotaxis irrespective of chemoattractants. Such an effect can be partly attributed to the perturbation of purine nucleotide biosynthesis.
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PMID:Inhibition of superoxide production and chemotaxis by methotrexate in neutrophils primed by TNF-alpha or LPS. 931 Jan 21


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