專題討論3:感控

S3-3
胃幽門螺旋桿菌致病與致癌機轉
Pathogenesis of Helicobacter pylori in Gastric Inflammation and Neoplasm
許秉寧 Ping-Ning Hsu
台大醫學院免疫學研究所
Graduate Institute of Immunology, College of Medicine, National Taiwan University, Taipei, Taiwan.

Helicobacter pylori(H. 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 induce sensitivity to 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 cells 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, initiate chemokine-mediated T lymphocyte trafficking into inflamed epithelium and induce the mucosal injury in Helicobacter infection. This topics 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 lymphoma.