Karabay G, Nacar A, Can F, Demirbilek M, Bacanli D, Take G, Yazici A C
Başkent University, Faculty of Medicine, Department of Histology and Embryology, Ankara, Turkey.
Acta Gastroenterol Belg. 2006 Apr-Jun;69(2):191-6.
The effect of H. pylori infection on gastric epithelial cell apoptosis and proliferation is contradictory. Using immunohistochemistry and electron microscopy, this study sought to demonstrate gastric epithelial changes (ie, apoptosis and proliferation) due to chronic H. pylori infection.
Eighteen female 6- to 8-week old Swiss Albino mice were inoculated intragastrically with 3 doses of 10(9) CFU/mL H. pylori prepared in a Brucella Broth in 5 days. Nine others served as a control group. At the end of 28 weeks, tissue specimens from the gastric antrum were excised and examined immunohistochemically (epithelial growth factor for regeneration and Caspase-3 for apoptosis) and electron microscopically. Immunohistochemical assessment was performed using the indirect peroxidase-antiperoxidase method.
In the H. pylori-infected group, EGF staining in gastric epithelium was found to be decreased significantly compared to that in control group (P < 0.001). Caspase-3 reactivity was commonly observed in surface epithelial cells and glandular epithelial cells in H. pylori-infected group and totally it was statistically significant compared to Caspase-3 staining in control group (P < 0.001). Electron micrograph images demonstrated numerous apoptotic cells with condensed chromatin.
Chronic H. pylori infection of 28 weeks' duration increases apoptosis in gastric epithelium; however, increased apoptosis does not induce proliferation.
幽门螺杆菌感染对胃上皮细胞凋亡和增殖的影响是相互矛盾的。本研究采用免疫组织化学和电子显微镜技术,试图证明慢性幽门螺杆菌感染引起的胃上皮变化(即凋亡和增殖)。
18只6至8周龄的雌性瑞士白化小鼠在5天内分3次胃内接种用布鲁氏肉汤制备的10(9) CFU/mL幽门螺杆菌。另外9只作为对照组。28周结束时,切除胃窦组织标本,进行免疫组织化学检查(用再生的上皮生长因子和凋亡的半胱天冬酶-3)和电子显微镜检查。免疫组织化学评估采用间接过氧化物酶-抗过氧化物酶法。
与对照组相比,幽门螺杆菌感染组胃上皮中的表皮生长因子(EGF)染色明显减少(P < 0.001)。在幽门螺杆菌感染组的表面上皮细胞和腺上皮细胞中普遍观察到半胱天冬酶-3反应性,与对照组的半胱天冬酶-3染色相比,总体上具有统计学意义(P < 0.001)。电子显微镜图像显示大量染色质浓缩的凋亡细胞。
持续28周的慢性幽门螺杆菌感染增加胃上皮细胞凋亡;然而,凋亡增加并未诱导增殖。