Adjuvant‐induced arthritis induces epithelial proliferation and differential expression of SVS2 and SVS3 in the seminal vesicles

Abstract

BACKGROUND: Rheumatoid arthritis (RA) is an inflammatory disease triggered by chronic and systemic activation of the immune system, with consequences for male fertility. However, the influence of RA on sexual accessory glands remains poorly investigated. OBJECTIVES: This study evaluated the late impact of adjuvant-induced arthritis (AIA) on the morphophysiology of the seminal vesicles and verified whether these effects can be influenced by androgen deprivation. MATERIALS AND METHODS: Adult male Wistar rats were allocated into four experimental groups and subjected to induction of AIA (via injection of Mycobacterium tuberculosis in the right hind paw), orchiectomy (ORX), both procedures (ORX/AIA), or neither (SHAM). Forty days after AIA induction, the seminal vesicles were processed for histopathological and morphometric-stereological analysis. Collagen deposition was measured, and immunostaining was conducted to determine PCNA, SVS2, and SVS3 expression. Serum testosterone was determined at 15 and 40 days after AIA induction. RESULTS: Body mass and wet weight of the seminal vesicles decreased in the AIA-induced and orchiectomized groups, and testosterone levels decreased in the AIA group. Collagen deposition in the seminal vesicle stroma increased in the orchiectomized rats, but not in the AIA rats. Induction of AIA promoted cellular proliferation in the distal region of the seminal vesicles in both intact and orchiectomized rats, and levels of two significant secretory proteins in the vesicle also changed with AIA: SVS2 increased, while SVS3 decreased. Conversely, orchiectomy decreased the expression of both SVS2 and SVS3. DISCUSSION: The late impact of AIA on seminal vesicle parameters appears to be compensated by an increase in epithelial cell proliferation and changes in secretory activity, in an androgen-dependent manner. CONCLUSION: The data suggest that transient arthritic hypoandrogenism and the direct action of joint inflammatory mediators may influence the seminal vesicle activity. Further research is required to better address the repercussions of arthritis on male fertility.