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首页> 外文期刊>Journal of Cellular Physiology >Biological effects of interleukin‐6 on Gingival Fibroblasts: Cytokine regulation in periodontitis
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Biological effects of interleukin‐6 on Gingival Fibroblasts: Cytokine regulation in periodontitis

机译：生物地理白介素6对牙龈的影响成纤维细胞:细胞因子调节在牙周炎

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Periodontitis is a bacterial infectious disease, and many inflammatory cytokines regulate periodontitis pathophysiology through a crosstalk between tissue cells and immune cells. Interleukin (IL)‐6 is an important cytokine involved in the regulation of host response to bacterial infection. Human Gingival Fibroblasts (HGFs) are the most abundant cells in gingival connective tissues. Various HGF responses to periodontal pathogens or inflammatory cytokines contribute to the development of periodontitis. Lipopolysaccharide derived from Porphyromonas gingivalis (Pg LPS) and IL‐1β significantly increase IL‐6 production in HGFs. However, IL‐6 cannot function in HGFs without the soluble form of the IL‐6 receptor (sIL‐6R), because HGFs do not express sufficient cell surface IL‐6R to bind appreciable levels of IL‐6. Importantly, sIL‐6R is essential for IL‐6 signaling in HGFs, and the sIL‐6R is produced by differentiated THP‐1 cells treated with IL‐6. Calprotectin, a heterodimer of S100A8 and S100A9, is released during inflammation and significantly induces IL‐6 production in HGFs via toll‐like receptor 4 (TLR4)/nuclear factor‐kappa B (NF‐κB) signals. Calprotectin also induces sIL‐6R production in differentiated THP‐1 cells. IL‐6 induces vascular endothelial growth factor (VEGF), matrix‐metalloproteinase‐1 (MMP‐1), and cathepsin L production in HGFs in the presence of sIL‐6R. Taken together, calprotectin‐induced IL‐6 production in HGFs may cause periodontitis progression through a crosstalk of fibroblasts and macrophages. There are many reports that examine how cytokines are released from HGFs to cause beneficial or harmful effects in inflamed periodontal lesions. This review explores the pathophysiology of periodontitis by focusing IL‐6‐mediated crosstalk of HGFs and macrophages.
机译：牙周炎是一种细菌传染病,和许多炎性细胞因子调节通过一个相声牙周炎病理生理学组织细胞和免疫细胞之间的关系。白介素6 (IL)检测是一个重要的细胞因子参与调节宿主反应细菌感染。(hgf)是最丰富的细胞在牙龈结缔组织。牙周病原体或炎性细胞因子对牙周炎的发展作出贡献。脂多糖是从Porphyromonasgingivalis有限合伙人(Pg)和IL 1β增加IL 6生产hgf。不能在hgf函数不溶性形式地理的IL 6受体(sIL量6 r),因为hgf做不表达足够的细胞表面IL 6 r绑定显著水平的IL 6。hgf对地理IL 6信号至关重要,和硅量6 r是由分化THP - 1细胞接受IL 6。S100A8和S100A9期间发布炎症,显著诱导IL 6通过人数的类受体4生产hgf(TLR4) /核因子量kappa B (NFκB)应承担的信号。Calprotectin也诱发sIL 6 r生产分化THP - 1细胞。血管内皮生长因子(VEGF),L生产hgf的银量6 r。综上所述,calprotectin检测诱导IL 6hgf的生产可能导致牙周炎发展成纤维细胞通过一个相声和巨噬细胞。研究如何从hgf释放细胞因子导致发炎有益或有害的影响牙周损伤。牙周炎的病理生理学IL 6的介导hgf的相声和巨噬细胞。

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