Chen G, Sordillo E M, Ramey W G, Reidy J, Holt P R, Krajewski S, Reed J C, Blaser M J, Moss S F
Department of Pathology, Columbia University, New York 10025, USA.
Biochem Biophys Res Commun. 1997 Oct 20;239(2):626-32. doi: 10.1006/bbrc.1997.7485.
Carriage of the bacterium H. pylori in the human stomach is associated with evidence of increased epithelial cell apoptosis. This may be of significance in the etiology of gastritis, peptic ulcers, and neoplasia. The ability of H. pylori to directly induce epithelial apoptosis was examined in vitro by fluorescence and electron microscopy, flow cytometry, and DNA fragmentation ELISA. The induction of apoptosis by H. pylori was time and concentration-dependent and inhibited by preventing direct bacterial-epithelial cell contact. Apoptosis was accompanied by increased expression of Bak, with little change in expression of other Bcl-2 family proteins. The expression of Bak was also increased in gastric biopsies from patients colonized by H. pylori. Thus, H. pylori induces gastric epithelial cell apoptosis, by a Bak-dependent pathway.
人类胃部幽门螺杆菌的携带与上皮细胞凋亡增加的证据相关。这在胃炎、消化性溃疡和肿瘤形成的病因学中可能具有重要意义。通过荧光和电子显微镜、流式细胞术以及DNA片段化ELISA在体外检测了幽门螺杆菌直接诱导上皮细胞凋亡的能力。幽门螺杆菌诱导的凋亡具有时间和浓度依赖性,并且通过阻止细菌与上皮细胞的直接接触而受到抑制。凋亡伴随着Bak表达的增加,而其他Bcl-2家族蛋白的表达变化不大。在幽门螺杆菌定植患者的胃活检组织中,Bak的表达也增加。因此,幽门螺杆菌通过依赖Bak的途径诱导胃上皮细胞凋亡。