Department of Laboratory Animal Medicine, College of Veterinary Medicine, Seoul National University, Seoul 151-742, Korea.
Microbiol Immunol. 2012 Nov;56(11):782-8. doi: 10.1111/j.1348-0421.2012.00505.x.
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.
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。