Differential response of neutrophils infiltrated to prostate gland in response to bacterial stimuli.

SCALERANDI, MV; GARCÍA, LN; LEIMGRUBER, C; PEINETTI, N; QUINTAR, AA; MALDONADO, CA

Buenos Aires

Congreso; IV LASID Meeting, LXIII Argentinean Society for Immunology Meeting, and II French Society for Immunology Meeting.; 2015

Sociedad Latinoamericana de Inmunología (LASID). Sociedad Argentina de Inmunología (SAI). French-Argentine Immunology Congress (FAIC).

There is scarce evidence about the role of testosterone on innate immunity and the early inflammatory response. In the present study, we characterized the neutrophil recruitment to the prostate in two acute models of protatitis, developed under different androgen status. Methods. Male Wistar rats with physiological (T-group) or low (castrated rats, OX-group) testosterone levels were subjected to acute prostatitis by intra-prostatic inoculation of E. coli (bacterial prostatitis-BP; OX+BP and T+BP groups) or lipopolysaccharide (LPS; OX+LPS and T+LPS groups). Animals were sacrificed 5 days after bacterial inoculation or 24 hours after LPS inoculation. The ventral prostates were harvested and processed for morphological analysis, assessment of infection, expression of βdefensin1 and neutrophils count.Results. The inoculation of bacteria and LPS into the prostate caused an acute inflammatory response with differences depending on the androgen status. The animals of T+BP group showed a significantly higher neutrophil infiltration compared to OX+BP group; however, OX+BP group exhibited higher infection reduction. The ultrastructural analysis confirmed the presence of phagocytosed bacteria in neutrophils in T+BP group, in line with the preservation of βdefensin1 over expression; meanwhile neutrophils in OX+BP group evidenced apoptotic features and were free of bacteria. In LPS-induced prostatitis, the number of infiltrating neutrophils per gland was higher in T+LPS than OX+LPS group (p=0.02). These results correlated with the largest inflammatory infiltrate observed in paraffin sections of T+LPS prostate gland. Conclusions. Testosterone favors the recruitment of neutrophils to the site of injury and modulates their ability to resolve bacterial prostatitis.