Increase in proliferation and apoptosis of gastric epithelial cells early in the natural history of Helicobacter pylori infection.
Increase in proliferation and apoptosis of gastric epithelial cells early in the natural history of Helicobacter pylori infection.
复制标题
DOI：
--
复制
发表时间：
1997-12
期刊：
影响因子：
--
通讯作者：
N. Jones;P. Shannon;E. Cutz;H. Yeger;P. Sherman
中科院分区：
文献类型：
--
作者：
N. Jones;P. Shannon;E. Cutz;H. Yeger;P. Sherman
儿童时期感染幽门螺杆菌是胃癌的一个关键危险因素。由于肿瘤发生涉及增殖和凋亡的失调，因此我们检查了幽门螺杆菌感染儿童的胃上皮细胞增殖和凋亡。比较幽门螺杆菌引起的胃炎、继发性胃炎和非炎症对照患者活检标本中胃窦上皮细胞的凋亡和增殖。通过免疫组织化学检查p53蛋白表达。在每组的表面上皮中均鉴定出凋亡细胞。幽门螺杆菌胃炎患者标本的细胞凋亡指数 (120 +/- 10) 高于继发性胃炎 (50 +/- 10) 和非炎症对照 (40 +/- 10，方差分析 P < 0.005)。幽门螺杆菌根除和胃炎消退后细胞凋亡减少（P < 0.02）。与继发性胃炎 (18.9 +/- 2.8) 和非炎症对照 (13.7 +/- 3.1，方差分析 P < 0.01) 相比，在幽门螺杆菌诱导的胃炎 (32.4 +/- 3.5；增殖标记指数 +/- SE) 中发现了扩大的增殖室。加速的细胞更新与 p53 过度表达相关（方差分析 P < 0.005）。 p53 的积累与细胞周期蛋白依赖性激酶抑制剂 p21 的表达无关。慢性感染自然史早期发生的细胞更新改变为与儿童获得感染相关的胃癌发展风险增加提供了解释。
Childhood acquisition of Helicobacter pylori is a critical risk factor for gastric cancer. Since tumorigenesis involves deregulation of proliferation and apoptosis, we examined gastric epithelial cell proliferation and apoptosis in H. pylori-infected children. Apoptosis and proliferation of gastric antral epithelial cells in biopsy specimens from patients with H. pylori-induced gastritis, secondary gastritis, and noninflamed controls were compared. p53 protein expression was examined immunohistochemically. Apoptotic cells were identified in the surface epithelium in each group. The apoptotic index was higher in specimens from patients with H. pylori gastritis (120 +/- 10) than secondary gastritis (50 +/- 10) and noninflamed controls (40 +/- 10, analysis of variance P < 0.005). Apoptosis decreased following H. pylori eradication and resolution of gastritis (P < 0.02). An expanded proliferative compartment was identified in H. pylori-induced gastritis (32.4 +/- 3.5; proliferative labeling index +/- SE) compared with secondary gastritis (18.9 +/- 2.8) and noninflamed controls (13.7 +/- 3.1, analysis of variance P < 0.01). The accelerated cell turnover was associated with p53 overexpression (analysis of variance P < 0.005). Accumulation of p53 was not associated with expression of the cyclin-dependent kinase inhibitor p21. The occurrence of altered cell turnover early in the natural history of chronic infection provides an explanation for the increased risk of gastric cancer development associated with childhood acquisition of infection.