CIBICI   14215
CENTRO DE INVESTIGACION EN BIOQUIMICA CLINICA E INMUNOLOGIA
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
The Th1 immune response underlying experimental autoimmune prostatitis induces chronic pelvic pain
Autor/es:
MOTRICH, RD; BRESER, ML; SANCHEZ, L; GODOY, GJ; RIVERO, VE
Lugar:
Mar del Plata
Reunión:
Congreso; LIX Reunión Científica Anual de la SAIC ? LXII Reunión Científica Anual de la SAI; 2014
Institución organizadora:
Sociedad Argentina de Investigación Clínica y Sociedad Argentina de Inmunologia
Resumen:
Pain is a hallmark in Chronic Pelvic Pain Syndrome patients in which prostate inflammation is present for at least 3 months. Although its etiology is still unclear, autoimmunity has been proposed as a cause. Our laboratory has pioneered the development of Experimental Autoimmune Prostatitis models that have reflected most disease features. Herein, we studied chronic pelvic pain development in parallel with autoimmune response and prostate inflammation in IL17-KO, IL12p70-KO, IL4-KO and wild type (C57BL/6) mice immunized with prostate antigens (PA) or saline (C). Animals were immunized on days 0 and 15. Pain was assayed as tactile allodynia using Von Frey filaments. Animals were euthanized and the specific immune response, prostate histopathology and infiltrating leukocytes were analyzed. Chronic pelvic pain was evidenced by increased allodynia responses in the pelvic region of PA-immunized wild type animals. Also, these animals showed elevated PA-specific immune responses with IFNg and IL17 secretion, together with marked prostate periglandular infiltration. Infiltrates were mainly composed of CD4 T cells and macrophages. Similar results were observed in immunized IL17-KO mice. Moreover, severe chronic pelvic pain was detected in immunized IL4-KO mice, which developed more exacerbated immune responses and disease. On the contrary, immunized IL12p70-KO mice developed mild to absent immune responses with high IL4 secretion, and neither infiltration nor damage in the prostate. As observed in wild type controls, these animals did not evidence tactile allodynia responses. Our results suggest that, as in patients, chronic pelvic pain is a consequence of prostate inflammation development. After PA immunization, a Th1 associated immune response develops and induces prostate infiltration and chronic pelvic pain. The absence of Th1 or Th2 cytokines respectively diminishes or enhances EAP susceptibility. On the other hand, IL17 showed to be dispensable for pathology induction.