Tu177 - Chronic Inflammation of the Male Genital Tract Affects Fertility by Decreasing Sperm Quality and Inducing Inflammation in the Female Genital Tract After Insemination

Fernando ferreyra – PhD Student, Clinical Biochemistry, Centro de Inmunología Clínica de Córdoba (CICC). CIBICI-CONICET; yair Chocobar – PhD Student, Clinical Biochemistry, Centro de Inmunología Clínica de Córdoba (CICC). CIBICI-CONICET; Daniela Paira – Postdoctoral Researcher, Clinical Biochemistry, Centro de Inmunología Clínica de Córdoba (CICC). CIBICI-CONICET; carolina Olivera – Postdoctoral Researcher, Clinical Biochemistry, Centro de Inmunología Clínica de Córdoba (CICC). CIBICI-CONICET; Virginia Rivero – Principal investigator, Clinical Biochemistry, Centro de Inmunología Clínica de Córdoba (CICC). CIBICI-CONICET; Rubén Motrich – Principal investigator, Clinical Biochemistry, Centro de Inmunología Clínica de Córdoba (CICC). CIBICI-CONICET

Abstract Text: Urogenital inflammation has been proposed as a cause of male infertility, suggested to account for at least 15% of male infertility cases. However, supporting evidence from animal models is scarce. Thus, we herein aimed to assess whether chronic prostatitis may cause infertility by either affecting sperm quality or impairing female genital immunoregulation using an animal model of experimental autoimmune prostatitis.

C57BL/6 male mice were immunized with prostate antigens (PA) or saline (C) on days 0 and 15 and the specific immune response, prostate histopathology and infiltrating leukocytes were assessed on day 26. At day 24, males were mated with BALB/c female mice and uterine immune changes that occur after insemination and different fertility parameters were analyzed.

Prostate-antigen-immunized mice showed chronic pelvic pain development and the induction of PA-specific Th1/Th17 responses associated to prostate and semen inflammation, and reduced sperm quality. Interestingly, female mice mated with PA-immunized mice showed significantly decreased fertility indexes and higher embryo loss rates with respect to controls. Remarkably, either early after copulation or during the peri-implantation window, significantly increased infiltrates of macrophages, dendritic cells, NK cells and CD4+ Teff cells, whereas altered number of Tregs, were observed in the uterine mucosa from these females with respect to controls, showing a shift towards uterine inflammation.

Our results indicate that PA-specific Th1/Th17 immune responses underlie chronic prostatitis development and causes semen inflammation. Of clinical interest, prostatitis significantly impairs fertility by reducing the fertilizing ability of sperm, altering the uterine immune response triggered after insemination, and increasing embryo loss.