Enhancement of Urinary Bladder Carcinogenesis by the Role of Chronic Bacterial Infection-induced Inflammation (Imunnohistochemical and Biochemical studies) | ||
| The Egyptian Journal of Hospital Medicine | ||
| Article 1, Volume 48, Issue 1, July 2012, Pages 334-347 PDF (956.75 K) | ||
| Document Type: Original Article | ||
| DOI: 10.21608/ejhm.2012.16238 | ||
| Authors | ||
| Gabri MS1; Ashmawy AM2; Ibrahim MA1; Hosny RM1 | ||
| 1Department of zoology and entomology, Faculty of Science, Helwan University | ||
| 2Department of cancer biology, National cancer institute, Cairo University. | ||
| Abstract | ||
| Background: Bacterial infections traditionally have not been considered major causes of cancer. Recently, however, bacteria have been linked to cancer by two mechanisms: induction of chronic inflammation and production of carcinogenic bacterial metabolites. The most specific example of the inflammatory mechanism of carcinogenesis is Escherichia coliinfection. E. coli has been epidemiologically linked to urothelial carcinoma of the urinary bladder by its propensity to cause lifelong inflammation. This inflammation is in turn thought to cause cancer by inducing cell proliferation and production of mutagenic free radicals and N-nitroso compounds. Material and methods: After each 3, 6 and 9 months of daily oral administration ofdibutyl amine (DBA) plus sodium nitrate (nitrosamine precursors) in drinking water, curcuma in grinding diet and bladder injection with E. coli, rats were sacrificed. The excited bladder were dissected, processed and stained with H&E and anti-Ki67 immunohistochemical stains. This was followed by Elisa for caspse-3 and statistical analysis. Results: The current results indicated that E. coli infection in the bladder tissues increases the carcinogenic ability of nitrosamine precursors through caused marked alteration in the form hyperplastic, dysplastic and metaplastic urothelium. Also, there was a statistically significant increase in ki67 immunoreactivity in urothelium. However, a statistically significant decrease in the concentration of caspase-3 in bladder tissue consequently caused the process of carcinogenesis. All these changes were less marked after curcuma treatment when compared with the group that not treated with curcuma. Conclusion: Bacterial infection of the urinary bladder may play a major additive and possible role in bladder carcinogenesis. Rhizome of curcuma may have a protective action during induction of urinary bladder tumors. | ||
| Keywords | ||
| Bladder carcinogenesis; E. coli; curcuma – DBA; Ki67-Immunohistochemistry; Caspase-3 | ||
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