Macrophage biology in the pathogenesis of Helicobacter pylori infection

Abstract

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.

Keywords:

• Macrophages
• Helicobacter pylori
• gastritis
• gastric cancer

Author contributions

NSL give the idea. XF drafted and edited the manuscript. XBX contributed to collect some data. NSL and YZ reviewed and revised the manuscript. All authors contributed to the article and approved the submitted version.

Disclosure statement

No potential competing interest was reported by the authors.

Additional information

Funding

This work was supported by the National Natural Science Foundation of China (82170580, 82260119), Natural Science Foundation of Jiangxi Province (20224ACB216004, 20225BCJ23021), and the Key Laboratory Project of Digestive Diseases in Jiangxi Province (2024SSY06101).