Abstract
Purpose Little is known of the etiology and pathogenesis of chronic inflammatory prostate diseases of noninfectious origin. In our experimental autoimmune rat model for chronic prostatic inflammation (CPI) we evaluated, in a time-course study, the specific cellular immune response to male accessory glands (MAG) and metabolic activity in the prostate gland. Results obtained in CPI rats were compared with data from rats immunized with kidney homogenate as well as from non-treated rats. Materials and Methods Specific cellular immune response against MAG antigen(s) was studied by delayed type hypersensitivity (DTH) and lymphocyte proliferation tests. The prostate 5 alpha-reductase activity was studied in prostate homogenates by thin layer chromatography (TLC). Results DTH values were positive in MAG treated rats sacrificed at days 7 and 28 after first immunization (FI) (p <or= to 0.05) in relation to kidney treated and non-treated rats. When we analyzed the proliferative responses to MAG antigen(s), an antigen specific proliferation, as shown by the mean [( 3) H]thymidine uptake (cpm), was observed in rats sacrificed on days 14 and 28 (p <or= to 0.05) after FI. The metabolic studies indicated that the 5 alpha-reductase activity decreased slightly in MAG treated groups at day 14 after FI and diminished significantly at the end of CPI development. Conclusion These data reveal that the prostatic endocrine cell destruction during CPI could be a consequence of immune/inflammatory cell mediated processes.
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