The contribution of toll-like receptor 2 on Helicobacter pylori activation of the nuclear factor-kappa B signaling pathway in gastric epithelial cells
The contribution of toll-like receptor 2 on Helicobacter pylori activation of the nuclear factor-kappa B signaling pathway in gastric epithelial cells
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Toll样受体2对幽门螺杆菌激活胃上皮细胞核因子-κB信号通路的贡献
DOI：
10.1016/j.micpath.2016.06.028
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发表时间：
2016-09-01
影响因子：
3.8
通讯作者：
Zhao, Jian
中科院分区：
文献类型：
--
作者：
Li, Shu;Cao, Mei;Zhao, Jian
幽门螺杆菌(Hp)是一种螺旋状革兰氏阴性细菌，可在胃粘膜中诱导免疫反应。Toll样受体(Toll-like Receptor，TLRs)通过识别细菌表面的保守分子模式，在介导炎症细胞因子中发挥重要作用。为探讨Toll样受体(Toll-like Receptor，TLR)在幽门螺杆菌(Hp)和大肠杆菌脂多糖(E.Coli)诱导下对胃粘膜上皮细胞Toll样受体(Toll-like Receptor，TLR)2、TLR4及相关炎性细胞因子表达的影响，探讨Toll样受体在识别和介导Hp感染炎症反应中的作用，并比较Hp和E.Coli TLRs表达的差异。针对TLR2和TLR4下降的特异性抑制剂也被使用。结果显示，幽门螺杆菌感染GES-1细胞后，TLR2的表达增加，而TLR4的表达不受Hp或TLR2小干扰RNA的影响。此外，幽门螺杆菌诱导的环氧合酶-2(COX-2)的分泌可被TLR2抑制，但不能抑制TLR4的分泌。综上所述，TLR2不仅在识别幽门螺杆菌方面发挥着比TLR4更重要的作用，而且在由幽门螺杆菌引发的炎性细胞因子的诱导方面也发挥着更为重要的作用。然而，TLR2和TLR4在介导对大肠杆菌内毒素的炎症反应中都是必需的。(C)2016爱思唯尔有限公司。保留所有权利。
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. (C) 2016 Elsevier Ltd. All rights reserved.