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)

Concentrations of five cytokines, GM-CSF, G-CSF, IL-1, IL-6 and IL-8, were determined within five compartments under four different conditions: at the time of a Caesarean section performed between 25 and 38 weeks' gestational age in normal pregnancy without uterine contraction (n = 12), in normal pregnancy with labour already established (n = 8), in pregnancy complicated by amniotic infection (n = 11), or under the conditions of preeclampsia with fetal intrauterine dystrophy (n = 13), cytokine concentrations were determined in fetal arterial and venous blood, in amniotic fluid, and in retroplacentally obtained maternal blood and peripheral maternal blood. With dystrophy, the concentrations of GM-CSF, G-CSF and IL-1 were about 20-50% lower (P < 0.01) in the amniotic fluid, and IL-6 and IL-8 were elevated in maternal peripheral blood (P < 0.01) but not within maternal retroplacental blood. Thus, preeclampsia/intrauterine dystrophy is characterized by reduction of some cytokines within the amniotic fluid compartment and concomitant reactive augmentations of other cytokines within the maternal and fetal organism. With amniotic fluid infection, concentrations of G-CSF, IL-6 and IL-8 were elevated in all compartments (P < 0.001) but GM-CSF and IL-1 showed a significant rise only within amniotic fluid and retroplacental maternal blood (P < 0.001), a rise that was apparently not transmitted to peripheral maternal or fetal blood. Care was taken to exclude the presence of uterine contractions in the group of controls, because this condition by itself causes severe elevation of cytokine concentrations, which are pronounced within amniotic fluid.
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PMID:Expression pattern of cytokines in the different compartments of the feto-maternal unit under various conditions. 874 67

It has been hypothesized that the development of cancer might partially result from a diminution of immunocompetence. Using ex vivo cytokine production by whole blood (WB) cells after polyclonal activation, we compared cytokine production levels of cancer patients to those of healthy controls. Seventeen patients without any prior treatment and attending the hospital for oncological surgery (for cancers of several origins) were enrolled in the study. WB was collected in heparinized tubes, diluted 1/10 in RPMI 1640 and incubated for 2, 4, 24, 48, and 72 h at 37 degrees C in the presence of 5 micrograms/ml PHA and 25 micrograms/ml LPS. Cytokine levels in the supernatant were measured by specific immunoassay kits. IL-10 levels after 24 h of culture, IFN-gamma and GM-CSF levels after 24 and 72 h of culture, and LIF levels after 72 h of culture were significantly lower in cancer patients than in healthy controls. No significant difference was observed for IL-1 beta, IL-2, IL-4, IL-8, and TNF-alpha production at any culture time. Our results suggest that the putative immunosuppression of cancer patients might be reflected by their reduced production of immunostimulated cytokines.
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PMID:Ex vivo cytokine production by whole blood cells from cancer patients. 876 14

While there is an extensive literature on cytokine regulation in vivo using human cell lines or peripheral blood monocytes, very little is known about cytokine regulation within the multicellular environment of inflammatory sites in vivo. We have previously shown that in rheumatoid synovial membrane cultures, a complex, but pathophysiologically relevant mixture of cells, the addition of a neutralizing anti TNF-alpha antibody inhibits the production of IL-1 and GM-CSF, indicating the presence of a cytokine 'cascade' in this inflammatory tissue. In this paper we demonstrate that the interactivities between cytokines in rheumatoid arthritis also extends to other cytokines, such as IL-6 and IL-8, and that within the IL-1 family it is IL-1 beta in particular which is downregulated by neutralizing TNF-alpha activity. The cytokine interactions are unidirectional, in that neutralization of TNF-alpha reduced IL-1 beta, IL-6 and IL-8 production, whereas treatment of the rheumatoid synovial membrane cells with a neutralizing concentration of the IL-1 receptor antagonist (IL-1ra) reduced IL-6 and IL-8 production but not TNF-alpha production. These results suggest a rationale for the profound anti-inflammatory effects and consequent clinical benefit noted in RA patients treated recently in clinical trials with a chimeric anti-TNF-alpha antibody in vivo.
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PMID:Modulation of proinflammatory cytokine release in rheumatoid synovial membrane cell cultures. Comparison of monoclonal anti TNF-alpha antibody with the interleukin-1 receptor antagonist. 878 87

The localization and production at the single cell level of 19 different human cytokines, IL-1 alpha, IL-1 beta, IL-1ra, IL-2, IL-3, IL-4, IL-5, IL-6, IL-8, IL-10, IL-13, TNF alpha, TNF beta, IFN gamma, GM-CSF, G-CSF, and TGF beta 1-3, were studied in cryopreserved tonsillar tissue using immunohistochemical staining. The cytokine producing cells, with the exception of IL-1 expressing cells, had a characteristic morphology due to the accumulation of cytokine onto the Golgi organelle. The production of each cytokine was localized to specific compartments in tonsillar tissue sections from children with tonsillar hypertrophy or recurrent tonsillitis in the resting state. Immunoregulatory cytokines such as IL-2, IL-3, IL-4, G-CSF, GM-CSF and TGF beta were produced in the extrafollicular area and entrapped on the cell membranes as well as in pudels in the extracellular matrix surrounding the producer cells. The dominating cytokines both in tissues from recurrent tonsillitis and tonsillar hypertrophy were GM-CSF, G-CSF, and TGF beta 1-3 which were synthezised predominantly in the reticular crypt site. IL-1 alpha, beta and IL-1ra, on the other hand, were localized to the surface and crypt epithelium and to scattered regions in the extrafollicular area. IL-2, IL-6, IFN gamma and IL-10 were found much more often in sections obtained from recurrent tonsillitis tissue compared with those from tonsillar hypertrophy. Reversely, an excessive production of IL-4 was noted in tonsillar hypertrophy compared with that in recurrent tonsillitis. Thus, concomitant production of multiple cytokines was evident with similarities but also differences in cytokine pattern between the two groups studied. The data suggest that T-cell mediated B-cell activation and differentiation take place in the extrafollicular area. Children with recurrent tonsillitis had a higher amount of B-cells and monocytes compared with children with tonsillar hypertrophy. However, the number of CD3, CD4, CD8 or cytoplasmic Ig-positive cells did not differ between the two groups.
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PMID:The production of immunoregulatory cytokines is localized to the extrafollicular area of human tonsils. 879 Jul 51

The present study was designed to investigate the in vitro effects of potential therapeutic agents on cytokine production by five HTVL-I-infected T cell clones (TCC) established from the ocular fluid of patients with HTLV-I uveitis. Each of the five HTLV-I-infected TCC was cultured at 1 x 10(6) cells/ml with or without an immunosuppressive agent (hydrocortisone, FK506, rapamycin, indomethacin, or prostaglandin E2) for 22 hr in humidified 5% CO2 in air at 37 C. The production of various cytokines in the culture supernatant from each TCC was measured by ELISA. The HTLV-I-infected TCC produced high amounts of IL-1 alpha, IL-3, IL-6, IL-8, TNF-alpha, IFN-gamma, and GM-CSF, and low but significant levels of IL-2 and IL-10 without any stimuli. Hydrocortisone severely depressed the production by these TCC of all the cytokines except for IL-2, which was slightly increased. Prostaglandin E2 depressed the production of IL-1 alpha, while it up-regulated the production of IL-6, TNF-alpha, and IFN-gamma. Rapamycin depressed the production of IL-6 and TNF-alpha, and FK506 depressed the production of TNF-alpha. Hydrocortisone also severely depressed the cytokine production by PHA-stimulated peripheral blood mononuclear cells obtained from healthy volunteers. Of the immunosuppressive agents tested, hydrocortisone exhibited the strongest suppression of cytokine production by HTLV-I-infected TCC. This result was in agreement with the in vivo effects of hydrocortisone in patients with HTLV-I uveitis. These TCC will be useful in investigating the effects of potential therapeutic agents for HTLV-I uveitis in vitro.
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PMID:In vitro effects of immunosuppressive agents on cytokine production by HTLV-I-infected T cell clones derived from the ocular fluid of patients with HTLV-I uveitis. 880 2

The immune response of T cells to self-HLA antigens on autologous non-T cells is known as the autologous mixed lymphocyte reaction (AMLR), and is defective in various diseases. We have investigated the effects of exogenous IL-10, a potential agent to treat various inflammatory diseases, on cytokine production induced by two-way AMLR in human peripheral blood mononuclear cells (PBMC). Effects of exogenous IL-4 were also investigated. IL-10 suppressed IL-6, IL-8, TNF-alpha and GM-CSF production when added at the beginning of culture and added 24 h after incubation. It abolished IL-1 alpha production only when added at the beginning of culture. IL-10 did not inhibit IL-3 production. The pattern of suppression by IL-10 of cytokine production induced by anti-CD3 mAb or PHA was similar to that induced by AMLR. Although IL-4 showed a largely similar pattern of inhibition when added at the beginning of culture, the level of inhibition was much lower than that of IL-10. IL-4 did not inhibit cytokine production when added 24 h after culture. These results indicate that IL-10, but not IL-4, is a potent inhibitor to cytokine production induced by two-way AMLR.
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PMID:Suppression by IL-10 and IL-4 of cytokine production induced by two-way autologous mixed lymphocyte reaction. 881 48

The bronchial epithelium produces cytokines that could contribute to inflammatory events in airways. In this study we determined the basal and TNFalpha stimulated productions of GM-CSF and IL-8 by human bronchial epithelial cells (HBEC) collected from 12 control and six asthmatic patients. Spontaneous and TNFalpha-induced GM-CSF or IL-8 released levels increased significantly with time. Epithelial cells from asthmatic patients spontaneously released high levels of GM-CSF (24 h). TNFalpha potentiated GM-CSF and IL-8 release in control subjects and only the IL-8 production in asthmatics. Nedocromil sodium, an antiinflammatory drug, and salbutamol, a beta2-agonist, are commonly used in asthma. They were evaluated on the spontaneous and TNF-induced expression of GM-CSF and IL-8 in cultured bronchial epithelial cells. Nedocromil sodium, at the concentration of 10(-6) M, reduced the TNF-induced increase in GM-CSF but not the IL-8 release. Salbutamol, at the concentration of 10(-6) or 10(-5) M, did not affect the constitutive or stimulated production of both cytokines.
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PMID:Granulocyte-macrophage colony stimulating factors (GM-CSF) and interleukin 8 (IL-8) production by human bronchial epithelial cells (HBEC) in asthmatics and controls. Lack of in vitro effect of salbutamol compared to sodium nedocromil. 882 Feb 49

Interleukin 1 (IL-1) potently activates human glomerular mesangial cells (HMC). In cytosolic extracts of IL-1-stimulated HMC or in anion exchange chromatography fractions we could not find any change in phosphorylation of myelin basic protein (MBP), a good substrate for extracellular regulated kinase (ERK). In contrast, IL-1 stimulated GST-jun kinase activity at least 10-fold. The jun kinase activity could be characterised as JNK1 and JNK2 at the protein and mRNA level. IL-1, TNF, UV light and osmotic stress, but not PMA, LPS, IL-3, IL-4, IL-6, IL-8, IL-10, IL-13, GM-CSF, PDGF, bFGF, TGF-beta and interferon-gamma were able to stimulate jun kinase activity in HMC, suggesting that jun kinase is selectively mediating signal transduction of the proinflammatory cytokines IL-1 and TNF as well as of cellular stress in HMC.
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PMID:Interleukin 1 activates jun N-terminal kinases JNK1 and JNK2 but not extracellular regulated MAP kinase (ERK) in human glomerular mesangial cells. 883 Jun 57

We have developed an enzyme-linked immunosorbent assay (ELISA) for the sequential analysis of multiple cytokines in limited volumes of biological fluids, including gingival crevicular fluid (GCF) and fibroblast culture supernatants (CS). GCF and CS samples were assayed for multiple cytokines, including IL-1 beta, IL-6, IL-8, GM-CSF and IFN gamma. Immulon 3 microplates were coated with a monoclonal antibody, and a rabbit polyclonal antibody was used to detect the cytokine of interest. Biological samples (200 microL) were added to an anti-IL-1 beta-coated plate and incubated, and 175 microL of each sample were replicate transferred to an anti-IFN gamma-coated plate containing 25 microL/well of diluent. This was repeated in an identical fashion with sequential replicate transfers to an anti-IL-8-coated and finally an anti-IL-6-coated plate. The cytokine standard was a pooled combination of the recombinant human cytokines that were included in the sequence. The plates were developed using an alkaline phosphatase-conjugated goat anti-rabbit IgG and NPP as the substrate. Individual ELISAs ranged in sensitivity from 30 to 2 pg/0.2 mL, with cross-reactivity between these cytokines of < 1%. Additionally, when the same samples were tested in the sequence ELISA vs. the individual ELISA, there was > 85% correlation between the two assays.
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PMID:Sequential ELISA for cytokine levels in limited volumes of biological fluids. 887 92

Cytokines released from activated alveolar macrophages and T-lymphocytes affect the accumulation of monocyte-macrophage-lineage cells and therefore play an important role in the formation of sarcoid granuloma. Although it is likely that certain monokines and lymphokines are involved in the development of sarcoid granulomas, the evidence for this is not unequivocal. In an attempt to clear critical cytokines in the development and maintenance of sarcoid granuloma, we have measured the level of seven cytokine mRNA (TNF-alpha, IL-6, IL-8, TGF-beta, PDGF-B, IFN-gamma, and GM-CSF) in cells obtained by BAL from sarcoidosis patients and normal subjects. To detect cytokine mRNA, we employed a reverse transcription-polymerase chain reaction. We report that the levels of TNF-alpha, IL-6, PDGF-B and GM-CSF mRNA were significantly increased in BAL cells from the patients with pulmonary sarcoidosis compared to controls. No significant differences were observed in the mRNA expression of IL-8, TGF-beta and IFN-gamma. A significant correlation of the expression of the mRNA levels of seven cytokines in the same patients with sarcoidosis was observed between IL-8 and TNF-alpha, PDGF-B, and IL-6, IL-8 and IL-6 and TFN-alpha and PDGF-B and IL-8. This finding indicates that at least these four cytokines are involved in the cytokine network at the local alveolar site of chronic granulomatous inflammation. This study adds a report to the literature that supports a role for cytokine, TNF-alpha, IL-6, PDGF and GM-CSF in particular, in the promotion and maintenance of sarcoid granulomatous inflammation.
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PMID:Increased expression of tumor necrosis factor-alpha, interleukin-6, platelet-derived growth factor-B and granulocyte-macrophage colony-stimulating factor mRNA in cells of bronchoalveolar lavage fluids from patients with sarcoidosis. 889 83


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