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目前关于幽门螺杆菌与巨噬细胞相互作用的研究。

Current research on the interaction between Helicobacter pylori and macrophages.

机构信息

Department of Gastroenterology, Beijing Friendship Hospital, Capital Medical University, Beijing, 100050, China.

Beijing Digestive Disease Center, State Key Laboratory of Digestive Health, National Clinical Research Center for Digestive Disease, Beijing, 100050, China.

出版信息

Mol Biol Rep. 2024 Apr 10;51(1):497. doi: 10.1007/s11033-024-09395-8.

DOI:10.1007/s11033-024-09395-8
PMID:38598010
Abstract

Helicobacter pylori (H. pylori) is a gram-negative bacteria with a worldwide infection rate of 50%, known to induce gastritis, ulcers and gastric cancer. The interplay between H. pylori and immune cells within the gastric mucosa is pivotal in the pathogenesis of H. pylori-related disease. Following H. pylori infection, there is an observed increase in gastric mucosal macrophages, which are associated with the progression of gastritis. H. pylori elicits macrophage polarization, releases cytokines, reactive oxygen species (ROS) and nitric oxide (NO) to promote inflammatory response and eliminate H. pylori. Meanwhile, H. pylori has developed mechanisms to evade the host immune response in order to maintain the persistent infection, including interference with macrophage phagocytosis and antigen presentation, as well as induction of macrophage apoptosis. Consequently, the interaction between H. pylori and macrophages can significantly impact the progression, pathogenesis, and resolution of H. pylori infection. Moreover, macrophages are emerging as potential therapeutic targets for H. pylori-associated gastritis. Therefore, elucidating the involvement of macrophages in H. pylori infection may provide novel insights into the pathogenesis, progression, and management of H. pylori-related disease.

摘要

幽门螺杆菌(H. pylori)是一种革兰氏阴性细菌,全球感染率为 50%,已知可引起胃炎、溃疡和胃癌。H. pylori 与胃黏膜内免疫细胞之间的相互作用是 H. pylori 相关疾病发病机制的关键。在 H. pylori 感染后,胃黏膜巨噬细胞数量增加,与胃炎的进展有关。H. pylori 诱导巨噬细胞极化,释放细胞因子、活性氧(ROS)和一氧化氮(NO),以促进炎症反应和消除 H. pylori。同时,H. pylori 已发展出逃避宿主免疫反应的机制,以维持持续感染,包括干扰巨噬细胞吞噬和抗原呈递,以及诱导巨噬细胞凋亡。因此,H. pylori 和巨噬细胞之间的相互作用可显著影响 H. pylori 感染的进展、发病机制和消退。此外,巨噬细胞作为治疗 H. pylori 相关胃炎的潜在靶点正在出现。因此,阐明巨噬细胞在 H. pylori 感染中的作用可能为 H. pylori 相关疾病的发病机制、进展和治疗提供新的思路。

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J Ethnopharmacol. 2023 Jun 28;310:116386. doi: 10.1016/j.jep.2023.116386. Epub 2023 Mar 14.
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MiR-1298-5p level downregulation induced by Helicobacter pylori infection inhibits autophagy and promotes gastric cancer development by targeting MAP2K6.幽门螺杆菌感染下调 miR-1298-5p 水平,通过靶向 MAP2K6 抑制自噬,促进胃癌发生。
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