CHRONIC INFLAMMATION OF THE MALE GENITAL TRACT IMPAIRS FERTILITY

Mar del Plata

Congreso; Reunión Anual de Sociedades de Biociencias 2022. SAIC-SAI-SAFIS; 2023

Sociedad Argentina de Inmunologia

Urogenital inflammation has been proposed as a cause of male infertilityas epidemiological studies revealed that it underlies at least15% of male infertility cases. However, supporting evidence fromanimal models is scarce. Herein, we analyzed the development ofExperimental Autoimmune Prostatitis (EAP) and its impact on fertility.C57BL/6 male mice were immunized with prostate antigens(PA) or saline on days 0 and 15. At day 24, males were mated withBALB/c female mice and different fertility parameters and uterineimmune changes that occur after insemination were analyzed. Malemice were euthanized on day 26 and the specific immune responseand prostate histopathology were assessed. Chronic pelvic paindevelopment was evidenced by increased allodynia responses inPA-immunized male mice. Furthermore, significantly increasedPA-specific lymphoproliferative responses with IFNg and IL17 secretion(p<0,0001) together with marked prostate periglandularmacrophage and CD4+ T cell infiltration and tissue inflammatorylesions were observed. None of these changes were present in controlmice. Interestingly, mating experiments revealed significantlydecreased fertility indexes and augmented rates of pre- and post-implantationembryo loss in female mice mated with PA-immunizedC57BL/6 males with respect to controls (p<0,05). Remarkably, thesefemales showed alterations in the immune cell changes that physiologicallyoccur in uterine mucosa after insemination such as significantlyincreased infiltration of macrophages, dendritic cells, NKcells and CD4+ T cells (p<0,05). Our results indicate that PA/specificTh1/Th17 immune responses underlie EAP associated chronic pelvicpain and prostate inflammation development. Of clinical interest,chronic inflammation of the prostate significantly impairs fertility byreducing the fertilizing ability of sperm, altering the uterine immuneresponse triggered after insemination, and increasing embryo loss.