[Molecular mechanisms of chronic gastric mucosal inflammation induced by Helicobacter pylori via immune evasion].

Helicobacter pylori (H. pylori) persistently colonizes the gastric mucosa and induces sustained inflammation, making it a major driver of the development and progression of chronic gastritis, peptic ulcer disease, and gastric cancer. Its pathogenicity does not rely on direct tissue damage inflicted by a single virulence factor, but rather on the coordinated actions of multiple factors, including cytotoxin-associated gene A (CagA), vacuolating cytotoxin A (VacA), lipopolysaccharide, and urease that disrupt the gastric epithelial barrier and perturb mucosal immune homeostasis. Concurrently, H. pylori modulates key immune recognition pathways, such as nuclear factor κB, mitogen-activated protein kinase, the NLRP3 inflammasome, and others, to reshape both innate and adaptive immune responses, thereby facilitating bacterial persistence and chronic infection. With deepening knowledge of H. pylori-host crosstalk, therapeutic strategies have evolved from mere pathogen elimination toward modulation of bacterial pathogenic processes and restoration of host immune homeostasis. In recent years, virulence-targeted approaches directed against CagA, VacA, the type Ⅳ secretion system, and colonization-associated factors, along with host-directed therapies that target inflammatory signaling cascades, have garnered increasing interest. This review summarizes the molecular underpinnings of H.pylori-host interactions, with a focus on virulence factor-mediated pathogenicity, host immune regulation, and the establishment of chronic inflammation. Moreover, we discuss emerging therapeutic modalities targeting pathogen-host interfaces and outline future directions, aiming to offer insights for precision prevention and treatment of H. pylori-associated diseases.