Macrophage biology in the pathogenesis of Helicobacter pylori infection
Xiao Fei1,2, Nianshuang Li1,2, Xinbo Xu1,2
1Department of Gastroenterology, Digestive Disease Hospital, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China.
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.
Insights
Helicobacter pylori infection causes gastric inflammation and cancer by evading macrophage defenses. Understanding these interactions is key to developing new treatments for H. pylori-associated diseases.
Area of Science:
- Immunology
- Gastroenterology
- Microbiology
Background:
- * Helicobacter pylori (H. pylori) infection is a primary cause of chronic gastric inflammation, peptic ulcers, and stomach adenocarcinoma.
- * Macrophages are critical innate immune cells involved in host defense against bacterial pathogens.
- * H. pylori employs specific mechanisms to evade phagocytosis, enabling gastric colonization and exacerbating preneoplastic pathology.
Purpose of the Study:
- * To review recent findings on macrophage interactions during H. pylori infection.
- * To elucidate the molecular mechanisms by which H. pylori influences macrophage polarization and function.
- * To highlight how these interactions impact the clinical outcomes of H. pylori infection.
Main Methods:
- * Literature review of studies investigating H. pylori and macrophage interactions.
- * Analysis of molecular pathways governing macrophage polarization (M1/M2) in response to H. pylori.
- * Examination of H. pylori's strategies for evading phagocytosis and promoting inflammation.
Main Results:
- * H. pylori promotes gastric inflammation via oxidative stress and resistance to macrophage phagocytosis.
- * H. pylori induces M1 macrophage polarization, contributing to inflammation.
- * M2 macrophages are implicated in promoting gastric cancer cell proliferation, invasion, and migration.
Conclusions:
- * Macrophage dysfunction is central to H. pylori pathogenesis, driving inflammation and cancer progression.
- * Understanding H. pylori-induced macrophage polarization is crucial for therapeutic strategies.
- * Targeting macrophage-pathogen interactions may offer novel approaches for managing H. pylori-associated gastric diseases.
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