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粘性放线菌的脂蛋白通过 TLR2 在人牙龈上皮细胞和巨噬细胞中诱导炎症反应。

Lipoproteins of Actinomyces viscosus induce inflammatory responses through TLR2 in human gingival epithelial cells and macrophages.

机构信息

Department of Oral Microbiology, Showa University School of Dentistry, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-8555, Japan.

出版信息

Microbes Infect. 2012 Sep;14(11):916-21. doi: 10.1016/j.micinf.2012.04.015. Epub 2012 May 4.

Abstract

Actinomyces viscosus has been suggested to be associated with periodontal disease. However, the pathogenicity of this bacterium is not known. In this study, we examined inflammation-inducing activity by A. viscosus. Whole cells and a lipophilic fraction of A. viscosus ATCC19246 induced production of interleukin-8 and tumor necrosis factor alpha from both human oral epithelial cells and human monocytoid cells. This cytokine production was blocked by lipoprotein lipase treatment of the lipophilic fraction. In addition, anti-Toll-like receptor 2 antibody blocked the cytokine production. These results suggest that lipoprotein of A. viscosus triggers inflammatory responses in periodontitis by activation of Toll-like receptor 2.

摘要

黏性放线菌被认为与牙周病有关。然而,这种细菌的致病性尚不清楚。在本研究中,我们研究了黏性放线菌的炎症诱导活性。黏性放线菌 ATCC19246 的全细胞和脂溶性部分可诱导人口腔上皮细胞和人单核细胞样细胞产生白细胞介素-8 和肿瘤坏死因子-α。脂溶性部分经脂蛋白脂酶处理后可阻断细胞因子的产生。此外,抗 Toll 样受体 2 抗体可阻断细胞因子的产生。这些结果表明,黏性放线菌的脂蛋白通过激活 Toll 样受体 2 引发牙周炎的炎症反应。

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