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IL-6 mRNA (il-6 + mrna)

Distribution by Scientific Domains
Medical Sciences100%

Terms modified by IL-6 mRNA

  • il-6 mrna expression
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    Selected Abstracts

    Quantitive cytokine mRNA expression profiles in the colonic mucosa of patients with steroid naïve ulcerative colitis during active and quiescent disease

    INFLAMMATORY BOWEL DISEASES, Issue 3 2009
    Reikei Matsuda MD
    Abstract Background: Cytokines have validated roles in the immunopathogenesis of inflammatory bowel disease (IBD). This study was to investigate the expressions of tumor necrosis factor (TNF)-,, interleukin (IL)-6, IL-8, and IL-10 mRNAs in the colonic mucosa of patients with ulcerative colitis (UC) during active and quiescent UC. Methods: At colonoscopy, biopsies were taken from inflamed and non-inflamed mucosa of patients with steroid-naive UC (n = 15), non-IBD inflammatory colitis controls (ICC, n = 6), and non-colitis controls (NCC, n = 14). The presence of extensive mononuclear cells and neutrophils infiltrate in the lamina propria, cryptitis, and epithelial damage defined an inflammatory lesion in the mucosa. Quantitative cytokine mRNA expressions in biopsies were measured by real-time polymerase chain reaction (PCR). Results: Of 15 UC patients, 3 remitted with 5-aminosalicylate and 11 received granulocytapheresis; of these, 10 remitted. At baseline, IL-6, IL-8, TNF-,, and IL-10 mRNAs were high in inflamed mucosa compared with NCC (P < 0.01). In active UC, IL-6, IL-8 and IL-10 mRNAs were high compared with non-inflamed mucosa (P = 0.03, P = 0.03, P < 0.05, respectively). Both TNF-, mRNA (P = 0.03) and IL-6 mRNA (P = 0.04) were higher in UC compared with ICC. Even in non-inflamed mucosa, IL-8 and TNF-, mRNA expressions were high compared with NCC. Both IL-6 and IL-8 mRNAs decreased to normal levels after granulocytapheresis. Conclusions: During active UC, all 4 cytokine mRNA levels were high; only IL-6 and IL-8 mRNAs decreased to normal levels during remission. IL-8 mRNA was high even at sites of endoscopically quiescent UC during active disease. Steroid naïve patients respond well to granulocytapheresis. (Inflamm Bowel Dis 2008) [source]

    Prostaglandin F2, upregulates interleukin-6 production in human gingival fibroblasts

    JOURNAL OF PERIODONTAL RESEARCH, Issue 2 2001
    Kazuyuki Noguchi
    Prostaglandin F2,(PGF2,) is a bioactive lipid mediator which has been suggested to be involved in the pathogenesis of periodontal disease. However, the roles of PGF2, in periodontal lesions are poorly understood. In the present study, we investigated the effect of PGF2, on interleukin (IL)-6 production in human gingival fibroblasts (HGF). PGF2,stimulated IL-6 production in a time- and concentration-dependent fashion. IL-1, and tumor necrosis factor ,(TNF,), proinflammatory cytokines, induced IL-6 production in a time-dependent manner, and PGF2,synergistically enhanced IL-6 production induced by IL-1, and TNF,. IL-6 mRNA was expressed in PGF2, -stimulated HGF, and PGF2, increased IL-6 mRNA levels induced by IL-1, and TNF,. Fluprostenol, a selective FP receptor agonist, could mimic PGF2, -induced IL-6 production. Since FP receptors are coupled to elevation of intracellular calcium and activation of protein kinase C (PKC), the mechanism of IL-6 production by PGF2, was investigated using TMB-8, an inhibitor of Ca2+ mobilization from intracellular stores, and calphostin C, an inhibitor of PKC. TMB-8 significantly suppressed PGF2, -induced IL-6 production, whereas calphostin C showed a stimulatory effect on PGF2, -induced IL-6 production. From these data, we suggest that PGF2, upregulates IL-6 production through FP receptors in HGF, that PGF2, synergistically enhances IL-6 production in IL-1,- and TNF,-stimulated HGF, and that PGF2, -induced IL-6 production may be dependent on intracellular Ca2+ mobilization and be downregulated by PKC activation. PGF2, may be involved in the pathogenesis of periodontal disease by enhancing IL-6 levels in periodontal lesions. [source]

    Insulin alters cytokine content in two pivotal organs after brain death: a porcine model

    ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 5 2008
    A. BARKLIN
    Background: To optimize the quantity and quality of organs available for transplantation, it is crucial to gain further insight into the treatment of brain dead organ donors. In the current study we hypothesized that insulin treatment after brain death alters cytokine content in the heart, liver, and kidney. Methods: Sixteen brain dead pigs (35,40 kg) were treated with either (1) no insulin [brain dead without insulin treatment treatment (BD)], or (2) insulin infusion intravenously (i.v.) at a constant rate of 0.6 mU/kg/min during 360 min [brain dead with insulin treatment (BD+I)]. Blood glucose was clamped at 4.5 mmol/l by infusion of 20% glucose. Blood samples for insulin, glucose, catecholamines, free fatty acids, and glucagon were obtained during the experimental period. Six hours after brain death biopsies were taken from the heart, liver, and kidney. These were analyzed for cytokine mRNA and proteins [tumor necrosis factor-, (TNF-,), interleukin (IL)-6, and IL-10]. Results: The BD+I compared with the BD animals had lower IL-6 concentrations in the right ventricle of the heart (P=0.001), in the renal cortex (P=0.04) and in the renal medulla (P=0.05), and lower IL-6 mRNA in the renal medulla (P=0.0002). Furthermore, the BD+I animals had lower concentrations in the renal medulla of IL-10 (P=0.01), and tended to have lower TNF-, in the renal cortex (P=0.06) than the BD animals. In the right ventricle of the heart TNF-, mRNA and IL-10 mRNA were higher in the BD+I than in the BD group (P=0.002 and 0.004). Conclusion: Insulin has anti-inflammatory effects on cytokine concentration in the heart and kidney after brain death. [source]

    ORIGINAL ARTICLE: The Role of IL-6, IL-10, TNF-, and its Receptors TNFR1 and TNFR2 in the Local Regulatory System of Normal and Impaired Human Spermatogenesis

    AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY, Issue 1 2009
    gorzata Bia
    Problem, To investigate the expression of genes coding for selected cytokines with antagonistic functions (IL-6, IL-10, TNF-,) as well as TNF-, receptors (TNFR1 and TNFR2) in correct spermatogenesis (normal proliferation), maturation arrest (proliferation inhibited) and testicular tumors (overgrowth). Method of study, Transcription levels of genes coding for IL-6, IL-10, TNF-,, TNFR1 and TNFR2 were quantitatively examined using a real-time RT-PCR. Results, Significantly higher amounts of IL-6 mRNA were observed in testicular tumor samples than in normal spermatogenesis or in some syndromes with maturation arrest (MA at spermatid level or SCOS), while IL-10 gene levels were fairly stable. In homogenates with maturation arrest, the expression of TNFR1 gene was markedly higher than in testicular tumors, while the opposite phenomenon was found in respect to TNFR2 gene. Conclusion, The results obtained indicate that changes in activities of intra-testicular cytokines may promote different distinct pathologies such as testicular cancer or infertility. [source]