Wilson K T, Fantry G T
Division of Gastroenterology, Department of Medicine, University of Maryland School of Medicine and Baltimore Veterans Affairs Medical Center, University of Maryland Medical Systems, Room N3W62, 22 South Greene Street, Baltimore, MD 21201, USA.
Curr Opin Gastroenterol. 1999 Jan;15(1):66-71. doi: 10.1097/00001574-199901000-00012.
Intensive investigation into the interactions of Helicobacter pylori with the human host during the period of this review has led to several important developments in our understanding of H. pylori pathogenesis. There is direct evidence to support a central role for bacterial adhesion to host gastric epithelial Lewis antigens. Adherence can result in activation of host signaling cascades, including tyrosine phosphorylation events. H. pylori induces an immune response that is skewed toward a T-helper cell (Th) 1 phenotype, and an insufficient Th2 response is associated with the inability of the host to eradicate the organism. An area of active investigation has been the induction of epithelial apoptosis, both in direct response to H. pylori and by T-cell mediated pathways. Although the consensus is that the cagA gene product is not involved in pathogenesis, the presence of the cag pathogenicity island is associated with increased gastric inflammation and decreased epithelial repair. Interestingly, infection with cagA+H. pylori appears to result in decreased prevalence of both gastroesophageal reflux disease and adenocarcinoma of the esophagus and cardia.
在本综述期间，对幽门螺杆菌与人类宿主相互作用的深入研究，使我们对幽门螺杆菌发病机制的理解有了几个重要进展。有直接证据支持细菌黏附于宿主胃上皮Lewis抗原起着核心作用。黏附可导致宿主信号级联反应的激活，包括酪氨酸磷酸化事件。幽门螺杆菌诱导的免疫反应倾向于T辅助细胞（Th）1表型，而Th2反应不足与宿主无法根除该病原体有关。一个活跃的研究领域是上皮细胞凋亡的诱导，这既可以是对幽门螺杆菌的直接反应，也可以通过T细胞介导的途径发生。虽然目前的共识是cagA基因产物不参与发病机制，但cag致病岛的存在与胃炎症增加和上皮修复减少有关。有趣的是，感染cagA +幽门螺杆菌似乎会导致胃食管反流病以及食管和贲门腺癌的患病率降低。
