Li Shu, Cao Mei, Song Liju, Qi Panpan, Chen Chong, Wang Xuege, Li Ningzhe, Peng Jingshan, Wu Daoyan, Hu Guoku, Zhao Jian
Key Laboratory of Biological Resource and Ecological Environment of Chinese Education Ministry, College of Life Science, Sichuan University, Chengdu, 610064, PR China.
Core Laboratory, School of Medicine, Sichuan Provincial People's Hospital Affiliated to University of Electronic Science and Technology of China, Chengdu, 610072, PR China.
Microb Pathog. 2016 Sep;98:63-8. doi: 10.1016/j.micpath.2016.06.028. Epub 2016 Jun 27.
Helicobacter pylori (H. pylori) is a spiral shaped gram-negative bacterium that induces immune responses in the gastric mucosa. Toll-like receptors (TLRs) play important roles in mediating inflammatory cytokines by recognition of conserved molecular patterns on bacteria. Changes in the expression of toll-like receptor (TLR) 2, TLR4 and the relative inflammatory cytokines were analyzed in normal gastric epithelial GES-1 cells following treatment with H. pylori or Escherichia coli lipopolysaccharide (E. coli LPS) in order to investigate the contribution of TLRs in recognizing and mediating the inflammatory response to H. pylori, and study the differences in TLRs' performance between H. pylori and E. coli. Specific inhibitors for the declines in TLR2 and TLR4 were also employed. The results showed that H. pylori infection increased TLR2 expression in GES-1 cells, but TLR4 remained unchanged regardless of H. pylori or TLR2 small interfering RNA treatment. Furthermore, the secretion of cyclooxygenase-2 (COX-2) induced by H. pylori was inhibited by declines in TLR2, but not in TLR4. In conclusion, TLR2 plays an even more important role than TLR4 not only in recognizing H. pylori, but also in the induction of inflammatory cytokines initiated by H. pylori. However, both TLR2 and TLR4 are necessary in mediating the inflammatory response to E. coli LPS.
幽门螺杆菌（H. pylori）是一种螺旋形革兰氏阴性菌，可在胃黏膜中诱导免疫反应。Toll样受体（TLRs）通过识别细菌上保守的分子模式在介导炎症细胞因子方面发挥重要作用。在用幽门螺杆菌或大肠杆菌脂多糖（E. coli LPS）处理正常胃上皮GES-1细胞后，分析了Toll样受体（TLR）2、TLR4及相关炎症细胞因子表达的变化，以研究TLRs在识别和介导对幽门螺杆菌的炎症反应中的作用，并研究幽门螺杆菌和大肠杆菌之间TLRs功能的差异。还使用了针对TLR2和TLR4下降的特异性抑制剂。结果显示，幽门螺杆菌感染增加了GES-1细胞中TLR2的表达，但无论幽门螺杆菌或TLR2小干扰RNA处理如何，TLR4均保持不变。此外，幽门螺杆菌诱导的环氧合酶-2（COX-2）分泌受到TLR2下降的抑制，但不受TLR4下降的抑制。总之，TLR2不仅在识别幽门螺杆菌方面，而且在幽门螺杆菌引发的炎症细胞因子诱导方面发挥着比TLR4更重要的作用。然而，TLR2和TLR4在介导对大肠杆菌LPS的炎症反应中都是必需的。
