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1	Signal transduction mechanisms regulating the activation, adhesion and migration of human eosinophils and T-lymphocytes in allergic inflammation. / CUHK electronic theses & dissertations collection January 2003 (has links) Ip Wai-Ki. / "July 2003." / Thesis (Ph.D.)--Chinese University of Hong Kong, 2003. / Includes bibliographical references (p. 261-290). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web. / Abstracts in English and Chinese. Eosinophils T-Lymphocytes Signal Transduction Inflammation NF-kappa B--metabolism MAP Kinase Signaling System Cell Adhesion Molecules--metabolism
2	Resveratrol modulates interleukin-1beta-induced phosphatidylinositol 3-kinase and nuclear factor kappaB signaling pathways in human tenocytes Busch, F., Mobasheri, A., Shayan, P., Lueders, C., Stahlmann, R., Shakibaei, M. January 2012 (has links) No / Resveratrol, an activator of histone deacetylase Sirt-1, has been proposed to have beneficial health effects due to its antioxidant and anti-inflammatory properties. However, the mechanisms underlying the anti-inflammatory effects of resveratrol and the intracellular signaling pathways involved are poorly understood. An in vitro model of human tenocytes was used to examine the mechanism of resveratrol action on IL-1beta-mediated inflammatory signaling. Resveratrol suppressed IL-1beta-induced activation of NF-kappaB and PI3K in a dose- and time-dependent manner. Treatment with resveratrol enhanced the production of matrix components collagen types I and III, tenomodulin, and tenogenic transcription factor scleraxis, whereas it inhibited gene products involved in inflammation and apoptosis. IL-1beta-induced NF-kappaB and PI3K activation was inhibited by resveratrol or the inhibitors of PI3K (wortmannin), c-Src (PP1), and Akt (SH-5) through inhibition of IkappaB kinase, IkappaBalpha phosphorylation, and inhibition of nuclear translocation of NF-kappaB, suggesting that PI3K signaling pathway may be one of the signaling pathways inhibited by resveratrol to abrogate NF-kappaB activation. Inhibition of PI3K by wortmannin attenuated IL-1beta-induced Akt and p65 acetylation, suggesting that p65 is a downstream component of PI3K/Akt in these responses. The modulatory effects of resveratrol on IL-1beta-induced activation of NF-kappaB and PI3K were found to be mediated at least in part by the association between Sirt-1 and scleraxis and deacetylation of NF-kappaB and PI3K. Overall, these results demonstrate that activated Sirt-1 plays an essential role in the anti-inflammatory effects of resveratrol and this may be mediated at least in part through inhibition/deacetylation of PI3K and NF-kappaB. Androstadienes Pharmacology Anti-inflammatory agents Non-Steroidal Apoptosis Drug effects Blotting Western Cells Cultured Collagen Metabolism Dose-response relationship Humans Inositol phosphates Interleukin-1beta Male Microscopy Electron Middle aged Mitochondria NF-kappa B/*metabolism Phosphatidylinositol 3-Kinase Antagonists & inhibitors Phosphorylation Proto-oncogene proteins c-akt Pyrazoles Pyrimidines Signal transduction Sirtuin 1 Stilbenes Tendons/cytology Time factors src-Family Kinases REF 2014
3	Molecular Regulation of Interleukin-13 and Monocyte Chemoattractant Protein-1 Expression in Human Mast Cells by Interleukin-1beta Lee, Steven A., Fitzgerald, S M., Huang, Shau K., Li, Chuanfu, Chi, David S., Milhorn, Denise M., Krishnaswamy, Guha 01 September 2004 (has links) Mast cells play pivotal roles in immunoglobulin (Ig) E-mediated airway inflammation, expressing interleukin (IL)-13 and monocyte chemoattractant protein-1 (MCP-1), which in turn regulate IgE synthesis and/or inflammatory cell recruitment. The molecular effects of IL-1beta on cytokine expression by human mast cells (HMC) have not been studied well. In this report, we provide evidence that human umbilical cord blood-derived mast cells (CBDMC) and HMC-1 cells express the type 1 receptor for IL-1. We also demonstrate that IL-1beta and tumor necrosis factor-alpha are able to induce, individually or additively, dose-dependent expression of IL-13 and MCP-1 in these cells. The induction of IL-13 and MCP-1 gene expression by IL-1beta was accompanied by the activation of IL-1 receptor-associated kinase and translocation of the transcription factor, nuclear factor (NF) kappaB into the nucleus. Accordingly, Bay-11 7082, an inhibitor of NF-kappaB activation, inhibited IL-1beta-induced IL-13 and MCP-1 expression. IL-1beta also induced IL-13 promoter activity while enhancing the stability of IL-13 messenger RNA transcripts. Dexamethasone, a glucocorticoid, inhibited IL-1beta-induced nuclear translocation of NF-kappaB and also the secretion of IL-13 from mast cells. Our data suggest that IL-1beta can serve as a pivotal costimulus of inflammatory cytokine synthesis in human mast cells, and this may be partly mediated by IL-1 receptor-binding and subsequent signaling via nuclear translocation of NF-kappaB. Because IL-1beta is a ubiquitously expressed cytokine, these findings have important implications for non-IgE-mediated signaling in airway mast cells as well as for innate immunity and airway inflammatory responses, such as observed in extrinsic and intrinsic asthma. active transport cell nucleus (drug effects genetics) cell line chemokine CCL2 (genetics immunology metabolism) dexamethasone (pharmacology) dose-response relationship drug drug synergism enzyme inhibitors (pharmacology) gene expression regulation (drug effects genetics) humans interleukin-1 (immunology metabolism pharmacology) interleukin-13 (genetics immunology metabolism) mast cells (drug effects immunology metabolism) NF-kappa B (metabolism) protein kinases (metabolism) RNA messenger (drug effects metabolism) receptors interleukin-1 (immunology metabolism) receptors interleukin-1 type I tumor necrosis factor-alpha (immunology metabolism pharmacology) Internal Medicine

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