Fei Xiao, Li Nianshuang, Xu Xinbo, Zhu Yin
Department of Gastroenterology, Digestive Disease Hospital, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China.
Jiangxi Provincial Key Laboratory of Digestive Diseases, Department of Gastroenterology, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi, China.
Crit Rev Microbiol. 2025 May;51(3):399-416. doi: 10.1080/1040841X.2024.2366944. Epub 2024 Jul 31.
Infection with induces chronic gastric inflammation, progressing to peptic ulcer and stomach adenocarcinoma. Macrophages function as innate immune cells and play a vital role in host immune defense against bacterial infection. However, the distinctive mechanism by which evades phagocytosis allows it to colonize the stomach and further aggravate gastric preneoplastic pathology. exacerbates gastric inflammation by promoting oxidative stress, resisting macrophage phagocytosis, and inducing M1 macrophage polarization. M2 macrophages facilitate the proliferation, invasion, and migration of gastric cancer cells. Various molecular mechanisms governing macrophage function in the pathogenesis of infection have been identified. In this review, we summarize recent findings of macrophage interactions with infection, with an emphasis on the regulatory mechanisms that determine the clinical outcome of bacterial infection.
感染[细菌名称未给出]会引发慢性胃炎症，进而发展为消化性溃疡和胃腺癌。巨噬细胞作为固有免疫细胞，在宿主抵御细菌感染的免疫防御中发挥着至关重要的作用。然而，[细菌名称未给出]逃避吞噬作用的独特机制使其能够在胃中定植，并进一步加剧胃肿瘤前病变。[细菌名称未给出]通过促进氧化应激、抵抗巨噬细胞吞噬以及诱导M1巨噬细胞极化来加剧胃炎症。M2巨噬细胞促进胃癌细胞的增殖、侵袭和迁移。已经确定了在[细菌名称未给出]感染发病机制中调控巨噬细胞功能的各种分子机制。在本综述中，我们总结了巨噬细胞与[细菌名称未给出]感染相互作用的最新研究发现，重点关注决定细菌感染临床结果的调控机制。
