幽门螺杆菌感染会诱发慢性胃炎症，进展为消化性溃疡和胃腺癌。巨噬细胞作为先天免疫细胞，在宿主免疫防御细菌感染方面发挥着至关重要的作用。然而，幽门螺杆菌逃避吞噬作用的独特机制使其能够在胃中定植，并进一步加重胃肿瘤前病变。幽门螺杆菌通过促进氧化应激、抵抗巨噬细胞吞噬作用和诱导 M1 巨噬细胞极化来加剧胃部炎症。 M2巨噬细胞促进胃癌细胞的增殖、侵袭和迁移。已经确定了幽门螺杆菌感染发病机制中控制巨噬细胞功能的多种分子机制。在这篇综述中，我们总结了巨噬细胞与幽门螺杆菌感染相互作用的最新发现，重点是决定细菌感染临床结果的调节机制。

Infection with H. pylori 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 H. pylori evades phagocytosis allows it to colonize the stomach and further aggravate gastric preneoplastic pathology. H. pylori 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 H. pylori infection have been identified. In this review, we summarize recent findings of macrophage interactions with H. pylori infection, with an emphasis on the regulatory mechanisms that determine the clinical outcome of bacterial infection.