W. Chronic bacterial infection and inflammation incite reactive hyperplasia in a mouse model of chronic prostatitis
Department of Surgery, Division of Urology, University of Wisconsin School of Medicine and Public Health, 600, Highland Ave, Madison, WI 53792, USA. The Prostate
(Impact Factor: 3.57).
01/2007; 67(1):14-21. DOI: 10.1002/pros.20445
Chronic inflammation is postulated to contribute to prostate carcinogenesis. We developed a mouse model of chronic prostatitis to test whether infection-induced chronic inflammation would incite reactive changes in prostatic epithelium.
Prostate tissues harvested from either phosphate-buffered saline (PBS) or E. coli-infected mice were evaluated for histological changes and immunostained for markers of oxidative stress and epithelial cell proliferation.
As compared to PBS-treated controls, mice infected with E. coli bacteria for 5 days showed foci of uniformly acute inflammation in the glandular lumen and a persistent inflammation at 12 weeks post-inoculation in the stroma. Prostatic glands showing varying degrees of atypical hyperplasia and dysplasia had stronger staining for oxidative DNA damage and increased epithelial cell proliferation than normal prostatic glands.
These data demonstrate that chronic inflammation induces reactive hyperplasia associated with oxidative stress injury and support the proposed linkage among inflammation, oxidative DNA damage, and prostate carcinogenesis.
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