Department of Internal Medicine, Taipei Medical University Shuang Ho Hospital, Taipei, Taiwan.
Cell Mol Immunol. 2010 Jul;7(4):255-9. doi: 10.1038/cmi.2010.2. Epub 2010 Mar 1.
Helicobacter pylori infection is associated with an inflammatory response in the gastric mucosa, leading to chronic gastritis, peptic ulcers, gastric carcinoma and gastric mucosa-associated lymphoid tissue (MALT) lymphomas. Recent studies have shown that apoptosis of gastric epithelial cells is increased during H. pylori infection. Apoptosis induced by microbial infections are factors implicated in the pathogenesis of H. pylori infection. The enhanced gastric epithelial cell apoptosis in H. pylori infection has been suggested to play an important role in the pathogenesis of chronic gastritis and gastric pathology. In addition to directly triggering apoptosis, H. pylori induces sensitivity to tumor-necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis in gastric epithelial cells via modulation of TRAIL apoptosis signaling. Moreover, H. pylori infection induces infiltration of T lymphocytes and triggers inflammation to augment apoptosis. In H. pylori infection, there was significantly increased CCR6(+)CD3(+ )T-cell infiltration in the gastric mucosa, and the CCR6 ligand, CCL20 chemokine, was selectively expressed in inflamed gastric tissues. These results implicate that the interaction between CCL20 and CCR6 may play a role in recruiting T cells to the sites of inflammation in the gastric mucosa during Helicobacter infection. Through these mechanisms, chemokine-mediated T lymphocyte trafficking into inflamed epithelium is initiated and the mucosal injury in Helicobacter infection is induced. This article will review the recent novel findings on the interactions of H. pylori with diverse host epithelial signaling pathways and events involved in the initiation of gastric pathology, including gastric inflammation, mucosal damage and development of MALT lymphomas.
幽门螺杆菌感染与胃黏膜的炎症反应有关，导致慢性胃炎、消化性溃疡、胃癌和胃黏膜相关淋巴组织（MALT）淋巴瘤。最近的研究表明，在幽门螺杆菌感染过程中，胃上皮细胞的凋亡增加。微生物感染诱导的细胞凋亡是与幽门螺杆菌感染发病机制相关的因素。幽门螺杆菌感染中增强的胃上皮细胞凋亡被认为在慢性胃炎和胃病理学发病机制中发挥重要作用。除了直接触发细胞凋亡外，幽门螺杆菌还通过调节 TRAIL 凋亡信号，诱导胃上皮细胞对肿瘤坏死因子（TNF）相关凋亡诱导配体（TRAIL）介导的凋亡敏感。此外，幽门螺杆菌感染诱导 T 淋巴细胞浸润并引发炎症以增强凋亡。在幽门螺杆菌感染中，胃黏膜中 CCR6（+）CD3（+）T 细胞浸润明显增加，并且 CCR6 配体 CCL20 趋化因子选择性地在炎症性胃组织中表达。这些结果表明，CCL20 和 CCR6 之间的相互作用可能在招募 T 细胞到幽门螺杆菌感染时胃黏膜炎症部位中发挥作用。通过这些机制，趋化因子介导的 T 淋巴细胞向炎症上皮的迁移被启动，并且幽门螺杆菌感染中的黏膜损伤被诱导。本文将综述幽门螺杆菌与宿主上皮信号通路的相互作用的最新研究发现，这些信号通路和事件参与了胃病理学的发生，包括胃炎症、黏膜损伤和 MALT 淋巴瘤的发展。
