Immune-enhancing effects of endogenous glucocorticoids on gastric macrophages contribute to the development of gastric inflammation and metaplasia

Abstract

Infection of the gastric mucosa with Helicobacter pylori is considered the major risk factor for gastric cancer, which remains a significant cause of cancer-related mortality worldwide. Gastric macrophages contribute to the development of gastric cancer by promoting chronic gastric inflammation and oxidative stress, consistent with a typical M1 macrophage phenotype (1). Gastric macrophages also contribute to gastric tumor progression following polarization to an M2 macrophage phenotype that can enhance angiogenesis and epithelial cell proliferation (1). However, the factors that control macrophage polarization and function in the gastric environment, particularly in the context of H. pylori infection, are still not fully understood.