Abstract
In rats, immunization with male accessory gland (MAG) extract promotes experimental autoimmune vesicle prostatitis. A specific mononuclear cell-mediated immune response and prostate androgen metabolism impairment in MAG-immunized rats were observed. The possibility that lymphocytic soluble factors (SoFs) can regulate the local steroid metabolism in these rats directly was studied. We investigated whether the SoFs released by MAG-sensitized lymphocytes are capable of modifying the prostatic androgen metabolism and whether they induce histologic lesions "in vivo" when they are inoculated, carried by liposomes, into untreated rats. "In vitro" enzymatic [3H]-5 alpha-dihydrotestosterone bioconversion and histologic studies were performed with prostates from SoF-treated rats (LK rats). The obtained 3 alpha/beta-hydroxysteroid-oxidoreductase activities showed that LK rat values were significantly lower than in controls: 79.0 +/- 2.5 vs 158.7 +/- 10.2 pmol/min/mg protein, respectively (P < 0.01). In the histologic studies, LK rat prostates showed focalized mononuclear infiltrates of various degrees, whereas control rats showed non-atypic modification of the gland. These results indicate that SoFs (probably total lymphokines) contribute significantly to the pathogenesis of experimental autoimmune prostatitis, involving a biochemical relationship between immune reaction and the androgenic enzymatic inhibition in the prostate.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
More From: American journal of reproductive immunology (New York, N.Y. : 1989)
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.