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首页> 外文期刊>BMC Microbiology >NF-κB activation by Helicobacter pylori requires Akt-mediated phosphorylation of p65
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NF-κB activation by Helicobacter pylori requires Akt-mediated phosphorylation of p65

机译：幽门螺杆菌激活NF-κB需要Akt介导的p65磷酸化

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Background The inflammatory response in Helicobacter pylori-infected gastric tissue is mediated by cag pathogenicity island (PAI)-dependent activation of nuclear factor-κB (NF-κB). Phosphatidylinositol 3-kinase (PI3K)/Akt signaling is known to play a role in NF-κB activation, but little information is available on the relationship between H. pylori and PI3K/Akt signaling in gastric epithelial cells. We examined whether H. pylori activates Akt in gastric epithelial cells, the role of cag PAI in this process and the role of Akt in regulating H. pylori-induced NF-κB activation. Results Phosphorylated Akt was detected in epithelial cells of H. pylori-positive gastric tissues. Although Akt was activated in MKN45 and AGS cells by coculture with cag PAI-positive H. pylori strains, a cag PAI-negative mutant showed no activation of Akt. H. pylori also induced p65 phosphorylation. PI3K inhibitor suppressed H. pylori-induced p65 phosphorylation and NF-κB transactivation, as well as interleukin-8 expression. Furthermore, transfection with a dominant-negative Akt inhibited H. pylori-induced NF-κB transactivation. Transfection with small interference RNAs for p65 and Akt also inhibited H. pylori-induced interleukin-8 expression. Conclusion The results suggest that cag PAI-positive H. pylori activates Akt in gastric epithelial cells and this may contribute to H. pylori-mediated NF-κB activation associated with mucosal inflammation and carcinogenesis.
机译：背景幽门螺杆菌感染的胃组织中的炎症反应是由cag致病岛（PAI）依赖性核因子-κB（NF-κB）激活介导的。磷脂酰肌醇3-激酶（PI3K）/ Akt信号已知在NF-κB激活中起作用，但是关于幽门螺杆菌与胃上皮细胞中PI3K / Akt信号之间关系的信息很少。我们检查了幽门螺杆菌是否激活了胃上皮细胞中的Akt，cag PAI在此过程中的作用以及Akt在调控幽门螺杆菌诱导的NF-κB激活中的作用。结果在幽门螺杆菌阳性胃组织的上皮细胞中检测到磷酸化的Akt。尽管通过与cag PAI阳性幽门螺杆菌菌株共培养在MKN45和AGS细胞中激活了Akt，但cag PAI阴性突变体却未激活Akt。幽门螺杆菌还诱导p65磷酸化。 PI3K抑制剂抑制幽门螺杆菌诱导的p65磷酸化和NF-κB反式激活以及白介素8表达。此外，显性阴性Akt的转染抑制幽门螺杆菌诱导的NF-κB反式激活。用p65和Akt的小干扰RNA转染也抑制幽门螺杆菌诱导的白介素8表达。结论结果表明，cag PAI阳性幽门螺杆菌可激活胃上皮细胞中的Akt，这可能与幽门螺杆菌介导的NF-κB活化有关，与黏膜炎症和致癌作用有关。

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