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)

Human polymorphonuclear leukocytes from normal subjects produced proinflammatory cytokines in response to stimulation with Cryptococcus neoformans yeast cells. The cytokines released after stimulation of neutrophils included interleukin-1beta (IL-1beta), IL-6, IL-8 and tumor necrosis factor alpha. The magnitude of the cytokine response was related to the yeast capsule size. Cells of a large-capsule isolate stimulated release of greater amounts of cytokine than did a thinly encapsulated isolate, which, in turn, stimulated release of greater amounts of cytokine than an acapsular isolate. Cytokine release was also stimulated by supernatant fluids from cryptococcal cells that were preincubated with 10% human serum, suggesting the generation of a soluble mediator. The major capsular polysaccharide, glucuronoxylomannan, stimulated release of tumor necrosis factor alpha, IL-1beta, and IL-8 in a dose-dependent fashion. These results differ from previous studies of cytokine secretion by human monocytes in several important respects, including the importance of encapsulation in stimulation of cytokine secretion and the ability of purified glucuronoxylomannan to induce cytokine secretion.
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PMID:Capsular polysaccharide of Cryptococcus neoformans induces proinflammatory cytokine release by human neutrophils. 875 10

Human T-cell lymphotropic virus type I (HTLV-I) is known to cause adult T-cell leukemia/T-cell lymphoma and tropical spastic paraparesis/HTLV-I-associated myelopathy. Recent seroepidemiologic, clinical, and virologic studies indicate that the virus is also related to a certain type of uveitis, which has been classified as uveitis without defined etiologies or idiopathic uveitis. According to the seroepidemiologic survey, the seroprevalence of HTLV-I in patients with idiopathic uveitis was significantly higher than that of two control groups, that is, patients with uveitis with defined etiologies and patients with nonuveitic ocular diseases. Clinically, the uveitis seen in HTLV-I carriers is characterized by moderate to severe cellular infiltration in the eye and by moderate retinal vasculitis, and the intraocular inflammation responds well to corticosteroid therapy. Interestingly, 25% of female patients with the disease had a previous history of Graves disease with hyperthyroidisms. The following virologic, molecular biologic findings suggest that cytokines produced by HTLV-I-infected T cells in the eye play the central role in the pathogenic mechanisms of the uveitis: (a) the virus load in the peripheral blood monocytes analyzed by the quantitative polymerase chain reaction methods was significantly greater in patients with the uveitis than in asymptomatic carriers, (b) the proviral DNA of HTLV-I and the gene expression of the virus at the mRNA level was detected in the infiltrating cells from the eyes of the patients, (c) the virus particles were detected by electron-microscopic examination in the T-cell clones established from the intraocular fluid of the patients, and (d) the HTLV-I-infected T cells produced a variety of cytokines without any stimuli, such as interleukin (IL)-1 alpha, IL-2, IL-3, IL-6, IL-8, IL-10, tumor necrosis factor alpha, interferon-gamma, and granulocyte-macrophage colony-stimulating factor. Based on the seroepidemiologic, clinical, and virologic data, the uveitis seen in HTLV-I carriers is considered to be a distinct clinical entity related to HTLV-I infection, and the disease is designated as HTLV-I uveitis.
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PMID:HTLV-I uveitis. 879 4

We measured the levels of soluble intercellular adhesion molecule-1 (sICAM-1), CD11a, CD11b, CD18, endotoxin, and various inflammatory cytokines to clarify the relationship between adhesive molecules and cytokines in sepsis. We studied 21 patients with sepsis (sepsis group) and 13 patients with trauma not complicated by infection (trauma group). The mean sICAM-1 level was significantly higher in the sepsis group than in the trauma group. No significant difference was observed in the CD11a, CD11b, and CD18 levels between the two groups. The sICAM-1 levels significantly correlated with the levels of endotoxin, tumor necrosis factor alpha (TNF-alpha), and IL-8, but CD11a, CD11b, and CD18 levels did not correlate with endotoxin or cytokine levels. These findings suggest that ICAM-1 production is induced by endotoxins and cytokines produced in excess by inflammatory reactions and that endotoxins and cytokines are involved in qualitative, but not quantitative changes in LFA-1 (CD11a/CD18) and Mac-1 (CD11b/CD18).
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PMID:Changes in adhesion molecule levels in sepsis. 882 72

We measured the levels of interleukin (IL) 1 beta, tumor necrosis factor alpha, and IL-8 in bronchoalveolar lavage fluid (BALF) and sera of patients with diffuse panbronchiolitis (DPB) before and after administration of erythromycin or roxithromycin. The pretreatment levels of IL-1 beta and IL-8 were significantly higher in the BALF of patients with DPB than in the BALF of patients with sarcoidosis and controls. The tumor necrosis factor alpha level was also higher than in controls, but not statistically significant. There was a significant correlation between percentage of neutrophils and IL-8 level in the BALF of DPB patients (r = 0.509; p < 0.05) on the one hand and between IL-1 beta and IL-8 on the other (r = 0.476; p < 0.04). Treatment for 1-24 months significantly reduced BALF levels of IL-1 beta and IL-8 of DPB patients in parallel with a reduction in BALF neutrophils. The serum level of IL-8 of DPB patients was higher, albeit insignificant, than that of controls and significantly lower than that in the BALF of the same patients (p = 0.0088). Serum IL-1 beta was below the detection limit. In addition, the concentration of IL-8 in alveolar macrophages obtained from 2 volunteers before and after oral erythromycin administration also decreased ex vivo. Our results indicate that IL-8 induces the migration of neutrophils to inflammatory sites. It is possible that the macrolides impair production and/or secretion of these cytokines, ultimately reducing neutrophil accumulation in the airway.
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PMID:Interleukin 1 beta, tumor necrosis factor alpha, and interleukin 8 in bronchoalveolar lavage fluid of patients with diffuse panbronchiolitis: a potential mechanism of macrolide therapy. 883 92

There have been few studies of cytokine expression in the gastric mucosa of patients with chronic gastritis. In the present study, to elucidate the expression of cytokines in the gastric mucosa and the immunopathological roles played by these cytokines in chronic gastritis, we investigated cytokine gene expression, by reverse transcription polymerase chain reaction, in gastric biopsy specimens obtained from 29 endoscopically normal patients with chronic gastritis. The cytokines examined and the mRNA positivity were: interleukin (IL)-1 beta (21%), IL-2 (0%), IL-3 (7%), IL-4 (41%), IL-5 (17%), IL-6 (53%), IL-8 (98%), interferon gamma (IFN-gamma) (69%), and tumor necrosis factor alpha (TNF-alpha) (24%). Although the histological severity of the gastritis was closely associated with Helicobacter pylori infection, the positivities of these cytokine mRNAs did not show a relationship with either H. pylori infection or with histological inflammation. Our findings suggest that the gastric mucosa responds to all exogenous antigens, including H. pylori, in the same fashion immunologically, and that these cytokines do not contribute to the induction of inflammation associated with H. pylori infection.
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PMID:Cytokine gene expression in the gastric mucosa: its role in chronic gastritis. 884 67

The involvement of bradykinin (BK) B1 and B2 receptors in cytokine-induced hyperalgesia has been studied in the rat. Intraplantar injections of interleukin (IL) 1 beta and tumor necrosis factor alpha (TNF alpha) induced thermal hyperalgesia, with in the the case of IL-1 beta, contralateral hyperalgesia also present. Subsequent to administration of IL-1 beta, but not after TNF alpha, des-Arg9-BK reduced the withdrawal latency in both ipsi- and contra-lateral paws. Mechanical hyperalgesia was also induced by IL-1 beta, IL-2, and IL-8 when injected into rat knee joints, whereas IL-6 and TNF alpha were without effect. Coadministration of des-Arg9,Leu8-BK prevented the development of the cytokine-induced hyperalgesia for the duration of the experiment (6 h), but HOE-140 only reversed the hyperalgesia for the 1st h. At 3.5 h after IL-1 beta, IL-2, or IL-8, administration of des-Arg9,Leu8-BK or HOE-140 (iv) completely reversed the hyperalgesia. Twenty-four hours after pretreatment with IL-1 beta, injection of des-Arg9-BK into the joint produced opposite effects, depending on the dose: at 50 pmol the hyperalgesia was reversed, but at 0.5 nmol there was further hyperalgesia. Both responses were blocked by B1 but not B2 receptor antagonists. These data suggest that both B1 and B2 receptors are involved in the induction and maintenance of cytokine-induced hyperalgesia. B1 receptors appear to play a more important role than B2 receptors in the development of mechanical hyperalgesia.
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PMID:Bradykinin B1 and B2 receptor mechanisms and cytokine-induced hyperalgesia in the rat. 884 17

Articular chondrocytes from nine arthritic patients, five infants, and Balb/c neonatal mice were analyzed for the presence of various cytokine mRNAs by a reverse transcriptase polymerase chain reaction (RT-PCR). Four cytokine mRNAs, interleukin (IL)-6, IL-8, IL-11, and macrophage colony stimulating factor (M-CSF), were detected in all human chondrocytes, regardless of source. IL-10, IL-12p35, and tumor necrosis factor alpha (TNF-alpha) transcripts were found in at least 12 of the 14 human samples. IL-13, granulocyte colony stimulating factor (G-CSF), granulocyte macrophage colony stimulating factor (GM-CSF), and TNF-beta mRNAs were found more predominantly in infant samples and in samples from patients with rheumatoid arthritis (RA) compared with samples from patients with osteoarthritis (OA). Another group of cytokine mRNAs, IL-1 (alpha, beta), IL-4, IL-5, and IL-7, were only weakly expressed in some human samples. The cytokine transcripts that were not found were IL-2, IL3, and interferon gamma (IFN-gamma). Because of the large array of cytokine transcripts detected, human chondrocyte preparations were further purified by reacting them with a monoclonal antibody specific to chondrocyte differentiation antigen and subjecting them to fluorescent-activated cell sorting. A similar array of cytokines was found between the sorted and unsorted chondrocytes, although TNF-alpha, G-CSF and GM-CSF transcripts appeared to be upregulated during the sorting process. Human chondrocytes that dedifferentiated into fibroblasts (a 40-day and a 77-day culture) no longer expressed mRNAs for IL-1, G-CSF, GM-CSF, and TNF-alpha, but all other cytokine mRNAs remained detectable. Although certain phenotypic characteristics were lost, including reactivity to chondrocyte-specific monoclonal antibodies and morphological features, chondrocytes in long-term culture still expressed cytokine mRNAs. As expected, more consistent results were obtained when seven preparations of chondrocytes from neonatal Balb/c mice were examined using available cytokine primers. They contained IL-1, IL-5, IL-6, IL-7, IL-12, GM-CSF, M-CSF, transforming growth factor beta (TGF-beta), TNF-alpha, and TNF-beta mRNAs but lacked IL-2, IL-3, IL-4, IL-10, and IFN-gamma mRNAs. Future experiments to define conditions by which these cytokine protein products are expressed are needed to help assess their roles in chondrocyte biology and in disease states.
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PMID:Cytokine mRNA repertoire of articular chondrocytes from arthritic patients, infants, and neonatal mice. 885 28

The objective of this study was to examine the age-dependent relationships between levels of inflammatory cytokines and collagen in human gingival inflammation. The gingival biopsies were obtained from 142 patients, divided into the following age groups: 6 to 14 years (prepubertal children); 18 to 35 years (young adults); 36 to 54 years (mature adults); and 55 years or above. The patients were also divided according to the severity of gingivitis. The tissues were analyzed for the contents of the inflammatory cytokines interleukin (IL)-1 beta, IL-6, IL-8, and tumor necrosis factor alpha (TNF-alpha) using specific ELISA kits, and interstitial collagen type I and type III using the ELISA method and specific antibodies. We found that in young adults, levels of IL-1 beta and IL-6 were significantly higher in inflamed than in non-inflamed gingiva. Total collagen in the young adults, however, was lower in inflamed than in non-inflamed gingiva. There was no significant difference in the levels of either IL-8 or TNF-alpha between inflamed and non-inflamed gingiva independent of age. No difference in the level of collagen type I between the inflamed and non-inflamed gingiva was found in any age groups. The level of collagen type III was lower in inflamed than in non-inflamed gingiva in both children and > or = 55 year group. The results indicate a disparity in the effect of age on the levels of cytokines and of collagen type I and type III in both clinically normal and inflamed gingiva.
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PMID:Levels of cytokines and collagen type I and type III as a function of age in human gingivitis. 886 18

The combined effects of hypoxia and interleukin 1, lipopolysaccharide, or tumor necrosis factor alpha on the expression of genes encoding endothelial constitutive and inducible nitric oxide synthases, endothelin 1, interleukin 6, and interleukin 8 were investigated in human primary pulmonary endothelial cells and whole pulmonary artery organoid cultures. Hypoxia decreased the expression of constitutive endothelial nitric oxide synthase (NOS-3) mRNA and NOS-3 protein as compared with normoxic conditions. The inhibition of expression of NOS-3 corresponded with a reduced production of NO. A combination of hypoxia with bacterial lipopolysaccharide, interleukin 1 beta, or tumor necrosis factor alpha augmented both effects. In contrast, the combination of hypoxia and the inflammatory mediators superinduced the expression of endothelin 1, interleukin 6, and interleukin 8. Here, we have shown that inflammatory mediators aggravate the effect of hypoxia on the down-regulation of NOS-3 and increase the expression of proinflammatory cytokines in human pulmonary endothelial cells and whole pulmonary artery organoid cultures.
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PMID:Lipopolysaccharide and interleukin 1 augment the effects of hypoxia and inflammation in human pulmonary arterial tissue. 890 7

Ehrlichia chaffeensis is a recently isolated minute gram-negative obligatory intracellular bacterium of monocytes/macrophages and is the etiologic agent of human monocytic ehrlichiosis. It is not known how macrophages respond when they encounter ehrlichiae in terms of cytokine production. In this study, we examined cytokine mRNA expression by incubating E. chaffeensis with THP-1 cells and performing competitive reverse transcription-PCR (RT-PCR). At 2 h postinfection, the levels of interleukin-1beta (IL-1beta), IL-8, and IL-10 mRNAs were significant but lower than those following Escherichia coli lipopolysaccharide (LPS) stimulation. Unlike the situation with E. coli LPS stimulation, however, IL-6, granulocyte-macrophage colony-stimulating factor (GM-CSF), and tumor necrosis factor alpha (TNF-alpha) mRNAs were not induced. Time course and dose-response studies confirmed the absence of IL-6, GM-CSF, and TNF-alpha mRNA induction with E. chaffeensis. Viable E. chaffeensis organisms were not required for IL-1beta IO, IL-8, and IL-10 mRNA induction, since heat-killed E. chaffeensis induced identical time course responses. IL-1beta, IL-8, and IL-10 mRNAs were detected for up to 21, 21, and 24 h postexposure with E. chaffeensis, respectively, which were shut off more rapidly than with LPS stimulation. Although heat treatment of E. chaffeensis had no effect, periodate treatment completely abolished the ability of E. chaffeensis to induce IL-1beta, IL-8, and IL-10 mRNAs. The capture enzyme-linked immunosorbent assay result corresponded with the RT-PCR results, showing that viable and heat-killed E. chaffeensis produced and secreted the same levels of IL-1beta and IL-8. IL-10 production was significantly reduced by heat treatment. Periodate-treated ehrlichiae did not induce production of any of the cytokines tested. Anti-CD14 monoclonal antibody and polymyxin B did not inhibit IL-1beta mRNA expression upon exposure to E. chaffeensis. The absence of TNF-alpha, IL-6, and GM-CSF mRNA induction may delay the development of a protective immune response, thereby allowing E. chaffeensis to set up residence in macrophages.
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PMID:Absence of tumor necrosis factor alpha, interleukin-6 (IL-6), and granulocyte-macrophage colony-stimulating factor expression but presence of IL-1beta, IL-8, and IL-10 expression in human monocytes exposed to viable or killed Ehrlichia chaffeensis. 892 90


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