Molecular Biological Studies on Cellular Proliferation and Apoptosis Induced by H. pylori

幽门螺杆菌可通过萎缩性胃炎和肠化生间接诱导胃癌发生，也可通过病原菌引起的细胞增殖和抗凋亡直接诱导胃癌发生。本研究从分子生物学水平探讨了(1)CagA对细胞内信号转导的激活作用和(2)幽门螺杆菌对细胞凋亡的抑制作用，揭示了cagPAI和CagA在这两种现象中的作用。通过根除幽门螺杆菌预防胃癌的临床研究最近在日本开始。然而，由于日本约有5000万人感染幽门螺杆菌，从经济角度和反流性食管炎加剧等并发症来看，不分青红皂白地根除幽门螺杆菌可能并不可行。如果我们能够区分胃癌的高危人群，了解幽门螺杆菌诱导的细胞增殖和抗凋亡机制将有助于预防胃癌的发生。

Gastric carcinogenesis may be induced by H. pylori indirectly through atrophic gastritis and intestinal metaplasia and directly through cellular proliferation and anti-apoptosis caused by the pathogen. We investigated in this study (1) the role played by CagA in the activation of intracellular signal transduction and (2) the suppression of apoptosis by H. pylori on molecular biological levels and revealed the role of cagPAI and CagA in each phenomenon. Clinical studies on the prevention of stomach cancer by H. pylori eradication has recently been started in Japan. However, since there are about 50 million people positive for H. pylori in Japan, indiscriminate eradication may not be feasible from the economic viewpoint and also concerning complications such as exacerbation of regurgitation esophagitis. Prevention of stomach cancer may become practical if we can discriminate those who are at a high risk for stomach cancer, which will be facilitated by the understanding of mechanisms underlying cellular proliferation and anti-apoptosis induced by H. pylori.