Prostate Fibrosis: A Consequence of Prostate Inflammation  and a Potential Etiology of Urinary Dysfunction

Bell-Cohn, Ashlee

doi:https://doi.org/10.21985/n2-hq7q-y348

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Prostate Fibrosis: A Consequence of Prostate Inflammation and a Potential Etiology of Urinary Dysfunction

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Fibrosis is a chronic pathology which commonly develops after chronic inflammation. Different specific kinds of inflammation have been linked to fibrosis across various tissues. When specifically occurring in the prostate, fibrosis can lead to urinary dysfunction. Prostate conditions that involve inflammation have also been linked to both prostate fibrosis and urinary dysfunction. Therefore, this study endeavored to explore and better understand the relationship between prostate inflammation, prostate fibrosis, and urinary dysfunction. While prostatic infection with a uropathogenic E.coli, called CP1, caused the development of chronic tactile allodynia in NOD/ShiltJ (NOD) but not C57BL/6 (B6) mice, both mice developed evidence of prostate inflammation, prostate fibrosis, and urinary dysfunction. Fibrosis was confirmed by the upregulation of fibrosis associated messenger RNAs (mRNAs), alpha smooth muscle actin immunohistochemistry, and collagen staining with picrosirius red. These findings were mainly focused in the dorsolateral lobes of the prostate. Both mouse strains also developed smaller, more frequent voiding patterns post-infection, examined via cystometry. B6 mice responded to CP1 infection with local production of type 2 cytokines (IL4 and IL13), while NOD mice did not, which may explain the tactile allodynia responses and level of collagen deposition. When mice lacking signal transducer and activator of transcription 6, STAT6, a transcription factor known to be important for the production and signaling of IL4 and IL13, were infected with CP1, fibrosis was attenuated. This study provides a potential model to study the development of infection-induced prostatic fibrosis and urinary dysfunction. This study also demonstrates that CP1-induced prostate fibrosis has a STAT6 dependent mechanism in B6 mice.

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