Helicobacter pylori induces apoptosis in Barrett's-derived esophageal adenocarcinoma cells
Helicobacter pylori induces apoptosis in Barrett's-derived esophageal adenocarcinoma cells
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DOI：
10.1016/s1091-255x(02)00129-4
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发表时间：
2003-01-01
影响因子：
3.2
通讯作者：
Rutten, MJ
中科院分区：
文献类型：
--
作者：
Jones, AD;Bacon, KD;Rutten, MJ
幽门螺杆菌可预防胃食管反流病患者Barrett上皮发育不良。本研究的目的是确定H.与正常细胞相比，pylori优先诱导Barrett's衍生癌细胞的凋亡。使巴雷特衍生的腺癌细胞系（OE 33）生长。H. pylori野生型、等基因vacA-、cagA-和picB/cagE-突变株在琼脂平板上生长。使用完整或超声处理的细菌处理正常和OE 33细胞24小时，并进行Hoechst染料结合以测量细胞凋亡。通过Western免疫印迹法测定FAS蛋白表达。用完整的H. pylori野生型菌株产生显著（P
Helicobacter pylori may protect against the development of dysplasia in Barrett's epithelium of patients with gastroesophageal reflux disease. The aim of this study was to determine whether H. pylori preferentially induces apoptosis in Barrett's-derived cancer cells compared to normal cells. A Barrett's-derived adenocarcinoma cell line (OE33) was grown. H. pylori wild-type, isogenic vacA-, cagA-, and picB/cagE- mutant strains were grown on agar plates. Intact or sonicated bacteria were used to treat normal and OE33 cells for 24 hours, and Hoechst dye binding was performed to measure apoptosis. FAS protein expression was determined by Western immunoblotting. OE33 cells treated with intact H. pylori wild-type strains produced significant (P