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Toll 样受体 2 在脆弱拟杆菌介导的鼠腹膜间皮细胞免疫反应中的关键作用。

Critical role of Toll-like receptor 2 in Bacteroides fragilis-mediated immune responses in murine peritoneal mesothelial cells.

机构信息

Department of Laboratory Animal Medicine, College of Veterinary Medicine, Seoul National University, Seoul 151-742, Korea.

出版信息

Microbiol Immunol. 2012 Nov;56(11):782-8. doi: 10.1111/j.1348-0421.2012.00505.x.

Abstract

In this study, the role of Toll-like receptor 2 (TLR2) in immune responses of murine peritoneal mesothelial cells against Bacteroides fragilis was investigated. Enzyme linked immunosorbent assay was used to measure cytokines and chemokines. Activation of nuclear factor κB (NF-κB-α) and mitogen-activated protein kinases (MAP kinases) was investigated by western blot analysis. B. fragilis induced production of interleukin-6, chemokine (C-X-C motif) ligand 1 (CXCL1) and chemokine (C-C motif) ligand 2 (CCL2) in wild type peritoneal mesothelial cells; this was impaired in TLR2-deficient cells. In addition, in response to B. fragilis, phosphorylation of inhibitory NF-κB-α and c-Jun N-terminal kinase mitogen-activated protein kinase (MAPK) was induced in wild type mesothelial cells, but not in TLR2-deficient cells,. Inhibitor assay revealed that NF-κB and MAPKs are essential for B. fragilis-induced production of CXCL1 and CCL2 in mesothelial cells. These findings suggest that TLR2 mediates immune responses in peritoneal mesothelial cells in response to B. fragilis.

摘要

在这项研究中,研究了 Toll 样受体 2(TLR2)在鼠腹膜间皮细胞对脆弱拟杆菌免疫反应中的作用。酶联免疫吸附试验用于测量细胞因子和趋化因子。通过 Western blot 分析研究核因子 κB(NF-κB-α)和丝裂原活化蛋白激酶(MAPK)的激活。脆弱拟杆菌诱导野生型腹膜间皮细胞产生白细胞介素 6、趋化因子(C-X-C 基序)配体 1(CXCL1)和趋化因子(C-C 基序)配体 2(CCL2);在 TLR2 缺陷细胞中,这种作用受损。此外,在对脆弱拟杆菌的反应中,野生型间皮细胞中诱导了抑制性 NF-κB-α和 c-Jun N-末端激酶丝裂原活化蛋白激酶(MAPK)的磷酸化,但 TLR2 缺陷细胞中没有。抑制剂试验表明,NF-κB 和 MAPK 对于脆弱拟杆菌诱导的间皮细胞中 CXCL1 和 CCL2 的产生是必不可少的。这些发现表明 TLR2 介导了腹膜间皮细胞对脆弱拟杆菌的免疫反应。

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