Division of Gastroenterology, Department of Internal Medicine.
Department of Developmental Biology, and.
J Clin Invest. 2020 May 1;130(5):2183-2185. doi: 10.1172/JCI135508.
Infection with the Gram-negative bacterium Helicobacter pylori remains the most important modifiable risk factor for the development of gastric cancer, a leading cause of cancer-related deaths worldwide. How the interactions between H. pylori and its host shape the gastric environment during chronic infection warrants further investigation. In this issue of the JCI, Palrasu et al. used human cell lines and mouse models to provide mechanistic insight into H. pylori's ability to delay apoptosis in gastric epithelial cells by actively driving the degradation of a proapoptotic factor, SIVA1. Their findings suggest that promoting the survival of gastric epithelial cells has implications not only for H. pylori pathogenesis but for host tumorigenesis.
感染革兰氏阴性细菌幽门螺杆菌仍然是导致胃癌发生的最重要的可改变的风险因素，胃癌是全球癌症相关死亡的主要原因。在慢性感染过程中，幽门螺杆菌与其宿主之间的相互作用如何塑造胃内环境，这仍需要进一步研究。在本期 JCI 中，Palrasu 等人利用人细胞系和小鼠模型，深入了解了幽门螺杆菌通过积极促进促凋亡因子 SIVA1 的降解来延迟胃上皮细胞凋亡的机制。他们的研究结果表明，促进胃上皮细胞的存活不仅对幽门螺杆菌的发病机制，而且对宿主的肿瘤发生都有影响。
