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)

An immunohistochemical technique was used to examine whether there was a colocalization of cytokine-specific receptors with cytokine-expressing cells. We have previously shown that there is extensive cytokine production and secretion in the rectal mucosa in shigellosis (interleukin 1 alpha [IL-1 alpha], IL-1 beta, IL-1ra, IL-4, IL-6, IL-8, IL-10, tumor necrosis factor alpha [TNF-alpha], TNF-beta, gamma interferon, granulocyte-macrophage colony-stimulating factor, and transforming growth factor beta [TGF-beta]) (R. Raqib, A. A. Lindberg, B. Wretlind, P. K. Bardhan, U. Andersson, and J. Andersson, Infect. Immun. 63:289-296, 1995; R. Raqib, B. Wretlind, J. Andersson, and A. A. Lindberg, J. Infect. Dis. 171:376-384, 1995). Kinetics for receptor expression was compared with that for cytokine synthesis in the inflamed rectal mucosa from Shigella-infected patients during acute (2 to 6 days after onset of diarrhea) and convalescent (30 to 40 days after onset) stages. Quantification of receptor expression was assessed by computer-assisted analysis of video microscopic images. A selective down-regulation of the receptors for gamma interferon, tumor necrosis factor (TNF receptor [TNFR] type I), IL-1 (IL-1 receptor [IL-1R] types I and type II), IL-3, IL-4, and TGF-beta (TGF-beta receptor type I) was observed at the onset of the disease, with a gradual reappearance during the convalescent stage. However, IL-2R, IL-6R, granulocyte-macrophage colony-stimulating factor receptor, TNFR type II, and TGF-beta receptor type II showed no change in expression during the study period and were comparable to controls. Cytokine receptors were predominantly located to the epithelial layer of the mucosal surface and crypts, with variable expression patterns in the lamina propria. A time-dependent kinetic curve was seen for the soluble IL-2R (sIL-2R), sIL-6R, and sTNFR types I and type II shed in stool at the acute stage similar to that observed for cytokine secretion in stool but at four- to six-times-lower concentration. In contrast, soluble receptor levels in plasma were 100-fold higher than the cytokine levels. The results suggest a dissociation in immune regulation between cytokine production and cytokine receptor expression. The down-regulation of the receptors in acute shigellosis was probably a consequence of cytokine-induced internalization and shedding of the receptors during signal transduction as well as due to programmed regulatory roles played by cytokines and the bacterial antigens.
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PMID:Down-regulation of gamma interferon, tumor necrosis factor type I, interleukin 1 (IL-1) type I, IL-3, IL-4, and transforming growth factor beta type I receptors at the local site during the acute phase of Shigella infection. 762 34

Immune parameters were examined in 188 patients who were exposed for more than 6 mo to pentachlorophenol-containing pesticides. Blood levels of pentachlorophenol, lymphocyte subpopulations, in-vitro responses to mitogenic and allogeneic stimulation, plasma neopterin levels, and plasma cytokine and cytokine receptor levels were determined. Impaired in-vitro lymphocyte stimulation responses were impaired in 65% of the patients. The likelihood of impaired lymphocyte stimulation increased significantly with levels of pentachlorophenol that exceeded 10 microliters/l (p < .05). Patients who had high blood levels of pentachlorophenol and abnormal lymphocyte stimulation also had increased proportions of blood monocytes in blood (p < .05), as well as increased IL-8 serum levels (p < .02). Eleven patients who had abnormal mitogen stimulation experienced decreased CD4/CD8 ratios of < 1.0; 5 of these patients had decreased CD4+ lymphocyte counts of < 500/microliters, and 3 patients had increased plasma neopterin of > 15 nmol/l. These results indicate that increased levels of pentachlorophenol in blood can lead to severe T lymphocyte dysfunction.
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PMID:Impaired in-vitro lymphocyte responses in patients with elevated pentachlorophenol (PCP) blood levels. 912 76

Inflammatory bowel disease (IBD) is characterized by T-cell activation and mucosal influx of inflammatory cells partly mediated by increased local release of cytokines and chemokines. Increased levels of activated platelets are reported in IBD. Activated platelets induce endothelial cells in vitro to secrete several cytokines and growth factors and to express adhesion molecules. This study investigates the expression of interleukin-1 (IL-1), IL-8 and granulocyte-macrophage colony-stimulating factor (GM-CSF) receptors on circulating platelets from patients with IBD and healthy controls and assesses the in vitro effect of various concentrations of IL-1 beta, IL-8 and GM-CSF on platelet activation in healthy controls. Flow cytometry was performed to quantify the percentage of platelets binding phycoerythrin (PE) labeled recombinant human IL-1 beta, IL-8 and GM-CSF. Platelet activation was assessed using fluorochrome labeled anti-GMP-140, an activation-dependent antigen. Results are expressed as percentage cytokine receptor expressing platelets (median and interquartile range IQR). Platelets from patients with IBD expressed significantly more cytokine receptors compared to healthy controls: IL-1R [8.7% (5.5-18.2) vs 3.1% (2.4-4.8), p < 0.05], IL-8R [22.5% (18.1-27.9) vs 8% (4.5-9.2), p < 0.001)], GM-CSFR [25.9% (16.1-39.2) vs 3.9% (2.7-3.9), p < 0.001]. The percentage of activated platelets was significantly increased after in vitro stimulation with IL-1 beta, IL-8 and GM-CSF. We conclude that cytokines and chemokines modulate platelet activation through specific, functional receptors which are upregulated in IBD.
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PMID:[Thrombocytes express functional cytokine receptors in patients with Crohn disease and ulcerative colitis]. 776 8

Hyperplasia of mesangial cells (MCs) precedes or accompanies progressive glomerular scarring, as is seen in chronic glomerulonephritis and diabetic glomerulosclerosis. The mechanisms causing in vivo MC proliferation and production of extracellular matrix (ECM) are incompletely understood. Cell culture studies have demonstrated that MCs produce as well as react to various polypeptide cytokines. Thus, MCs have the potential to generate soluble mediators which can, in a paracrine fashion, attract and activate inflammatory cells (platelets, monocyte-macrophages, granulocytes), for example by IL-6, IL-8, MCP-1 and GM-CSF, and exert autocrine effects on MCs themselves, such as by promoting MC proliferation (by PDGF, IL-1, IL-6) or ECM production (by TGF-beta, IL-1). Recent in vitro results have revealed that specific non-soluble ECM components (collagen III, IV; laminin) also affect MC behavior with regard to adhesion, cell replication, ECM production as well as their response to cytokines. The latter effect appears to be mediated by alterations of cytokine receptor expression on MCs in the presence of the ECM components. "Cross-talk" between MCs, cytokines, ECM and inflammatory cells is likely to be of great importance in the regulation of the MC phenotype and may play a prominent role in the initiation and progression of glomerular inflammation. First in vivo findings in rats with experimental glomerular disease and in kidney biopsies from patients with glomerulonephritis have supported this concept by demonstrating abnormal MC expression of cytokines, their receptors and ECM proteins. These MC products may promote the recruitment and activation of inflammatory cells and perpetuate MC proliferation as well as ECM build-up.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cytokines and mesangial cells. 846 21

Topical steroid treatment is a common therapy for psoriasis. Steroids are known to bind to specific cytoplasmic receptors and to influence gene expression. We investigated the effects of the novel steroid derivative mometasone furoate on the expression of putative target genes in normal human epidermal cells (KC). Gene expression was measured by semiquantitative mRNA-PCR. In addition, cytokine receptor characteristics were assessed by ligand binding studies. We found a dose-dependent downregulation of proinflammatory mediators (IL-8, TNF alpha). Genes involved in growth regulation (HER-2, p53) were also modulated. IL-8 binding to KC was inhibited. We conclude that modulation of the expression of cytokine, cytokine receptor and growth factor genes may contribute to the antipsoriatic action of steroids.
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PMID:Novel steroid derivative modulates gene expression of cytokines and growth regulators. 852 52

We present a detailed analysis of cytokine expression patterns of the two permanent human bone marrow stromal cell lines, L87/4 and L88/5. These cell lines, previously established in our laboratory, are highly radiotolerant without cell detachment and support long-term cultures of CD(34+)-enriched human cord blood cells. RT-PCR analysis of 22 different cytokines or cytokine receptor mRNAs showed an almost identical expression pattern in the two stromal cell lines compared to primary human Dexter-type stroma. Since stromal feeder lines employed in long-term cultures usually are irradiated and grown in media containing corticosteroids, we analyzed the impact of irradiation and dexamethasone on cytokine production in the two cell lines by RT-PCR, Northern blot analysis, bioassays, and RIAs. By RT-PCR analysis, constitutive mRNA expression of c-kit, G-CSF, GM-CSF, IL-1 beta, IL-6, IL-7, IL-8, IL-11, Kit ligand (KL), LIF, M-CSF, MIP-1 alpha, TGF-beta, and TNF-alpha was demonstrated in both cell lines, with L87/4 a more potent cytokine producer than L88/5. Northern blot data showed an increase in mRNA levels for GM-CSF, IL-1 beta, and LIF by irradiation and IL-1 alpha treatment in both cell lines. IL-1 alpha-induced GM-CSF, IL-1 beta, IL-6, IL-11, and LIF mRNA levels were reduced by the addition of dexamethasone, whereas dexamethasone had no influence on the amounts of IL-1 alpha-induced G-CSF mRNA. L87/4 and, to a lower extent, L88/5 cells showed dexamethasone-dependent increases in KL mRNA, while KL mRNA levels were not stimulated by IL-1 alpha.
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PMID:Constitutive and modulated cytokine expression in two permanent human bone marrow stromal cell lines. 853 85

Sepsis is a constellation of clinical signs and symptoms resulting from excessive systemic host inflammatory response to infection. This inflammatory response is largely mediated by cytokines, which are released into the systemic circulation. Plasma concentrations of specific cytokines, TNF alpha, IL-1 beta, IL-6 and IL-8 are frequently elevated in human sepsis and cytokine concentrations correlate with severity and outcome of sepsis. In addition to pro-inflammatory cytokines, soluble cytokine receptors, cytokine receptor antagonists and counter-inflammatory cytokines are also produced in large quantities in patients with sepsis; however, the specific role of these molecules in sepsis remains undefined. A complex interaction of cytokines and cytokine-neutralizing molecules probably determines the clinical presentation and course of sepsis. Intervening in this sequence of events to modify the host inflammatory responses may prove to be a beneficial treatment strategy for sepsis, but currently tested anticytokine therapies have been largely unsuccessful.
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PMID:Sepsis and cytokines: current status. 870 20

We investigated the effects of hypoxemia +/- reoxygenation (H/R) on matrix protein regulation of polymorphonuclear leukocyte (PMN) IL-1beta types I and II, TNF-alpha (p60, p80), and IL-8R expression compared with normoxic controls. H/R reduction IL-1beta type I, TNF-alpha (p80), and IL-8R expression compared with hypoxic levels. Neither fibronectin nor laminin effected cytokine receptor expression during normoxia, but both fibronectin and laminin significantly reduced IL-1beta type I, TNF-alpha (p80), and IL-8R expression during hypoxia. Following H/R, both fibronectin and laminin significantly reduced IL-1beta type I, TNF-alpha (p80), and IL-8R expression during hypoxia. Following H/R, both fibronectin and laminin significantly increased TNF-alpha (p60, p80) and IL-8R expression. Cross-linking of adherent PMN very late antigen (VLA)-5 and VLA-6 receptors resulted in a progressive increase in TNF-alpha (p60, p80) and IL-8R expression during hypoxia; cross-linking of adherent PMN VLA-5 and and VLA-6 receptors resulted in a progressive increase in TNF-alpha (p60, p80) and IL-8 receptors following H/R. Cross-linkage of IL-1betaR type I, TNF-alphaR (p80), and IL-8R during hypoxia and H/R resulted in increased and subsequently decreased O2- production and degranulation. Inhibition of reduced nicotinamide adenine dinucleotide phosphate oxidase activation with diphenyleneiodonium following hypoxia but before reoxygenation prevented the decreases in IL-1beta types I and II, TNF-alpha (p80), and IL-8R expression that was seen following H/R alone. These results demonstrate that, during hypoxia and H/R, integrin signaling via alpha5beta1, and alpha6beta1 increases and subsequently decreases the expression of PMN cytokine receptors.
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PMID:Regulation of polymorphonuclear leukocyte cytokine receptor expression: the role of altered oxygen tensions and matrix proteins. 887 61

Glucocorticoids inhibit the expression and action of most cytokines. This is part of the in vivo feed-back system between inflammation-derived cytokines and CNS-adrenal produced corticosteroids with the probable physiological relevance to balance parts of the host defence and anti-inflammatory systems of the body. Glucocorticoids modulate cytokine expression by a combination of genomic mechanisms. The activated glucocorticoid-receptor complex can (i) bind to and inactivate key proinflammatory transcription factors (e.g. AP-1, NF kappa B). This takes place at the promotor responsive elements of these factors, but has also been reported without the presence of DNA; (ii) via glucocorticoid responsive elements (GRE), upregulate the expression of cytokine inhibitory proteins, e.g. I kappa B, which inactivates the transcription factor NF kappa B and thereby the secondary expression of a series of cytokines; (iii) reduce the half-life time and utility of cytokine mRNAs. In studies with triggered human blood mononuclear cells in culture, glucocorticoids strongly diminish the production of the 'initial phase' cytokines IL-1 beta and TNF-alpha and the 'immunomodulatory' cytokines IL-2, IL-3, IL-4, IL-5, IL-10, IL-12 and IFN-gamma, as well as of IL-6, IL-8 and the growth factor GM-CSF. While steroid treatment broadly attenuates cytokine production, it cannot modulate it selectively, e.g. just the TH0, the TH1 or the TH2 pathways. The production of the 'anti-inflammatory' IL-10 is also inhibited. The exceptions of steroid down-regulatory activity on cytokine expression seem to affect 'repair phase' cytokines like TGF-beta and PDGF. These are even reported to be upregulated, which may explain the rather weak steroid dampening action on healing and fibrotic processes. Some growth factors, e.g. G-CSF and M-CSF, are only weakly affected. In addition to diminishing the production of a cytokine, steroids can also often inhibit its subsequent actions. Because cytokines work in cascades, this means that steroid treatment can block expression of the subsequent cytokines. The blocked cytokine activity does not depend on a reduced cytokine receptor expression; in fact available in vitro investigations show that while the cytokine expression is blunted, its receptor is upregulated. The cellular studies presented here may represent the maximum potential of steroids to modulate cytokine expression in human mononuclear cells. It remains to be determined by clinical-experimental studies how effective cytokine modulation can be achieved in situ in inflamed bowel by systemic or by topical steroid therapy. Such studies may also answer whether a blocked cytokine production/action is the key or just a secondary mechanism behind the unique efficacy of steroids in active inflammatory bowel disease.
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PMID:Cytokine modulation by glucocorticoids: mechanisms and actions in cellular studies. 889 6

Burkitt's lymphoma (BL) represents a high malignant B cell tumour. It has been proposed that cytokines are responsible for some of the characteristics of BL. We have analysed a panel of different BL and lymphoblastoid cell lines (LCLs) for the expression of cytokines, including: IL 1 alpha, IL 1 beta, IL2, IL3, IL4, IL6, IL8, IL10, TNF alpha and TNF beta and for the soluble cytokine receptor for IL2 (slL2R). Our results show that expression of IL8, IL10, TNF alpha or TNF beta was detected frequently in several of the Burkitt or lymphoblastoid cell lines. There was a correlation between Epstein-Barr virus (EBV) infection and cytokine protein production. Our results suggest that EBV promote the expression of IL8, IL10, TNF alpha and TNF beta.
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PMID:Promotion of IL8, IL10, TNF alpha and TNF beta production by EBV infection. 891 15


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