Chronic bacterial infection and inflammation incite reactive hyperplasia in a mouse model of chronic prostatitis
JE Elkahwaji, W Zhong, WJ Hopkins… - The Prostate, 2007 - Wiley Online Library
JE Elkahwaji, W Zhong, WJ Hopkins, W Bushman
The Prostate, 2007•Wiley Online LibraryBackground 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. Methods 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. Results As compared to PBS‐treated controls, mice infected with …
developed a mouse model of chronic prostatitis to test whether infection‐induced chronic
inflammation would incite reactive changes in prostatic epithelium. Methods 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. Results As compared to PBS‐treated controls, mice infected with …
Background
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.
Methods
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.
Results
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 persitent 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.
Conclusions
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. Prostate 67:14–21, 2007. © 2006 Wiley‐Liss, Inc.
Wiley Online Library