MOTRICH RUBEN DARIO
Congresos y reuniones científicas
Título:
Pathogenic consequences in semen quality and male fertility of an autoimmune response against the prostate gland: from animal models to human disease
Autor/es:
MOTRICH, RUBEN DARIO; GATTI, G; PONCE, A; MACKERN OBERTI, JP; RIERA, CM; MACCIONI, M; RIVERO, VE
Lugar:
Teheran, Iran
Reunión:
Congreso; Royan International Twin Congress: 7th Congress on Reproductive Biomedicine and 2nd Congress on Stem Cell Biology & Technology.; 2005
Institución organizadora:
The Royan Institute (Theran, Iran), European Society of Human Reproduction and Embryology (ESHRE), Middle East Fertility Society (MEFS) y The British Andrology Society (BAS)
Resumen:
Introduction: We have recently found an autoimmune etiology in approximately 35 % of chronic non bacterial prostatitis (CNBP) patients, the most frequent form of prostatitis observed, since they exhibit INFg-secreting lymphocytes specific to prostate antigens. Interestingly, this particular group of patients, but not the rest of CNBP patients, also presented striking abnormalities in their semen quality.
Materials and methods: Autoimmune prostatitis was induced in Wistar rats and the cell and humoral autoimmune response against prostate antigens was studied. At the same time, sperm quality parameters, such as sperm concentration, motility, viability and Hypo-Osmotic Swelling test were measured in semen samples obtained by electroejaculation and in epididymal sperm. Sperm apoptosis was studied in both, seminal and epididymal sperm. Citric acid, fructose and alpha-glycosidase levels were assayed as biomarkers of sexual accessory glands. Measurements of prostate-specific autoantibodies, TNF-alpha, NO, ROS and IFN-gamma levels in seminal plasma were performed. Mixture experiments with autoimmune seminal plasma and normal sperm were also assayed.
Results: As previously observed in patients, a marked reduction in sperm concentration, almost null sperm motility and viability and an increased percentage of apoptotic spermatozoa were detected in semen samples from animals with the disease. Decreased levels of citric acid but normal fructose and alpha-glycosidase were observed, indicating an impaired prostate functionality and normal seminal vesicles and epididymal function. Prostate specific autoantibodies as well as elevated levels of NO, ROS, TNF-a and IFN-g were also detected in their seminal plasma. In contrast, epididymal spermatozoa remained intact, indicating that sperm damage occurs at the moment of joining of prostate secretion to sperm cells during ejaculation. These results were further supported by experiments in which mixture of normal sperm cells with autoimmune seminal plasma were performed.
Conclusion: As in patients, autoimmunity against the prostate gland seriously compromise the sperm quality. We hypothesize that sperm damage in experimental autoimmune prostatitis can be the triggered by the inflammatory milieu, originally produced by an autoimmune response in the prostate; a diminished prostate functionality, evidenced by reduced levels of citric acid in semen or by both mechanisms simultaneously. Once more, we suggest that autoimmunity to prostate may have consequences on fertility.
Materials and methods: Autoimmune prostatitis was induced in Wistar rats and the cell and humoral autoimmune response against prostate antigens was studied. At the same time, sperm quality parameters, such as sperm concentration, motility, viability and Hypo-Osmotic Swelling test were measured in semen samples obtained by electroejaculation and in epididymal sperm. Sperm apoptosis was studied in both, seminal and epididymal sperm. Citric acid, fructose and alpha-glycosidase levels were assayed as biomarkers of sexual accessory glands. Measurements of prostate-specific autoantibodies, TNF-alpha, NO, ROS and IFN-gamma levels in seminal plasma were performed. Mixture experiments with autoimmune seminal plasma and normal sperm were also assayed.
Results: As previously observed in patients, a marked reduction in sperm concentration, almost null sperm motility and viability and an increased percentage of apoptotic spermatozoa were detected in semen samples from animals with the disease. Decreased levels of citric acid but normal fructose and alpha-glycosidase were observed, indicating an impaired prostate functionality and normal seminal vesicles and epididymal function. Prostate specific autoantibodies as well as elevated levels of NO, ROS, TNF-a and IFN-g were also detected in their seminal plasma. In contrast, epididymal spermatozoa remained intact, indicating that sperm damage occurs at the moment of joining of prostate secretion to sperm cells during ejaculation. These results were further supported by experiments in which mixture of normal sperm cells with autoimmune seminal plasma were performed.
Conclusion: As in patients, autoimmunity against the prostate gland seriously compromise the sperm quality. We hypothesize that sperm damage in experimental autoimmune prostatitis can be the triggered by the inflammatory milieu, originally produced by an autoimmune response in the prostate; a diminished prostate functionality, evidenced by reduced levels of citric acid in semen or by both mechanisms simultaneously. Once more, we suggest that autoimmunity to prostate may have consequences on fertility.
