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). |
© Acta Gastro-Enterologica Belgica. |