AI‐2 represses CagA expression and bacterial adhesion, attenuating the Helicobacter pylori‐induced inflammatory response of gastric epithelial cells,Helicobacter

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AI‐2 represses CagA expression and bacterial adhesion, attenuating the Helicobacter pylori‐induced inflammatory response of gastric epithelial cells
Helicobacter ( IF 4.3 ) Pub Date : 2021-01-05 , DOI: 10.1111/hel.12778
Yancheng Wen _{1,

2} , Hongming Huang _{1,

2} , Tiechen Tang ₃ , Huang Yang _{1,

2} , Xi Wang _{1,

2} , Xi Huang _{1,

2} , Yingying Gong _{1,

2} , Xiaoyan Zhang _{1,

2} , Feifei She _{1,

2}

Affiliation

Helicobacter pylori (H. pylori) infection of gastric epithelial cells induces inflammatory response. Outer membrane proteins (OMPs), Type 4 secretion system (T4SS) encoded by cagPAI, and the effector protein CagA are involved in the pathogenesis of H. pylori. H. pylori possesses a gene encoding LuxS which synthesizes AI‐2, a quorum sensing signal molecule. The aim of this study was to investigate the role of AI‐2 in the expression of virulence factors and the inflammatory response of gastric epithelial (AGS) cells induced by H. pylori.

中文翻译：

AI-2抑制CagA表达和细菌粘附，减轻幽门螺杆菌诱导的胃上皮细胞炎症反应

幽门螺杆菌（H. pylori）感染胃上皮细胞会诱发炎症反应。外膜蛋白 (OMP)、由cag PAI编码的 4 型分泌系统 (T4SS)和效应蛋白 CagA 参与了幽门螺杆菌的发病机制。H. pylori拥有一个编码 LuxS 的基因，该基因合成 AI-2，一种群体感应信号分子。本研究的目的是研究 AI-2 在毒力因子表达和幽门螺杆菌诱导的胃上皮 (AGS) 细胞炎症反应中的作用。

更新日期：2021-03-09

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