Host genetic factors respond to pathogenic step-specific virulence factors of Helicobacter pylori in gastric carcinogenesis.

摘要: The interindividual differences in risk of Helicobacter pylori (H. pylori)-associated gastric cancer involve significant heterogeneities both host genetics and H. strains. Several recent studies proposed a distinct sequence for exerting its virulence the stomach: (i) adhering to colonizing surface epithelial cells, (ii) evading attenuating defense, (iii) invading damaging mucosa. This review focuses on several key issues that still need be clarified, such as which factors are involved three pathogenic steps, genes respond step-specific factors, whether and/or how corresponding genetic variations influence carcinogenesis. Urease, BabA SabA adhesion-step, PGN LPS immune evasion-step, CagA, VacA Tipα mucosal damage-step were documented play an important role pathogenicity infection. There is evidence further supporting potentially functional polymorphisms directly responding these susceptibility carcinogenesis, especially urease-interacting HLA class II genes, BabA-interacting MUC1, PGN-interacting NOD1, LPS-interacting TLR4, CagA-interacting PTPN11 CDH1. With continuous improvement understanding profile pylori-associated person at increased may benefit from aspects efforts: prevent infection with vaccine targeting certain factor; eradicate by blocking psychopathological characteristics factors; adjust physiological function resist carcinogenic or interrupt cellular signal transduction interplay between each step, subjects precancerous lesions stomach.