Macrophage biology in the pathogenesis of infection.

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.