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Apoptosis and proliferation in gastric epithelium due to Helicobacter pylori : An immunohistochemical and ultrastructural study

Journal Volume 69 - 2006
Issue Fasc.2 - Original articles
Author(s) G. Karabay, A. Nacar, F. Can, M. Demirbilek, D. Bacanlı, G. Take, A.C. Yazıcı
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Başkent University, Faculty of Medicine, Departments of (1) Histology and Embryology, (2) Microbiology, (3) Laboratory Animal Breeding and Research Center and (4) Biostatistics.

The effect of H. pylori infection on gastric epithelial cell apoptosis and proliferation is contradictory. Using immunohisto- chemistry and electron microscopy, this study sought to demon- strate gastric epithelial changes (ie, apoptosis and proliferation) due to chronic H. pylori infection. Methods : Eighteen female 6- to 8-week old Swiss Albino mice were inoculated intragastrically with 3 doses of 109 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 immunohis- tochemically (epithelial growth factor for regeneration and Caspase-3 for apoptosis) and electron microscopically. Immuno- histochemical assessment was performed using the indirect peroxi- dase-antiperoxidase method. Results : 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 com- monly observed in surface epithelial cells and glandular epithelial cells in H. pylori-infected group and totally it was statistically sig- nificant compared to Caspase-3 staining in control group (P < 0.001). Electron micrograph images demonstrated numerous apoptotic cells with condensed chromatin. Conclusion : Chronic H. pylori infection of 28 weeks' duration increases apoptosis in gastric epithelium; however, increased apoptosis does not induce proliferation. (Acta gastroenterol. belg., 2006, 69, 191-196).

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