Th1 but not Th17 Cells are Essential for Prostate Inflammation and Chronic Pelvic Pain Development in an Experimental Model of Chronic Prostatitis/Chronic Pelvic Pain Syndrome

Event Abstract Back to Event Th1 but not Th17 Cells are Essential for Prostate Inflammation and Chronic Pelvic Pain Development in an Experimental Model of Chronic Prostatitis/Chronic Pelvic Pain Syndrome Ruben D. Motrich1, Maria L. Breser1, Leonardo R. Sanchez1, Gloria J. Godoy1, Immo Prinz2 and Virginia E. Rivero1* 1 Universidad Nacional de Cordoba, Centro de Investigaciones en Bioquímica Clínica e Inmunología (CIBICI) - Consejo Nacional de Investigaciones Cientificas y Tecnicas (CONICET), Facultad de Ciencias Químicas, Argentina 2 Institute of Immunology. Hannover Medical School., Germany Pain and inflammation in the absence of infection are hallmarks in Chronic Prostatitis/Chronic Pelvic Pain Syndrome (CP/CPPS) patients. Its etiology is unclear and autoimmunity has been proposed as a cause. Our laboratory has pioneered the development of Experimental Autoimmune Prostatitis (EAP) models that have reflected most disease features and have long been used for studying CP/CPPS. Herein, we studied the autoimmune response and prostate inflammation induction together with chronic pelvic pain development in EAP using IL-12p40-KO, IL-4-KO, IL-17-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. Prostate antigen (PAg)-immunized C57BL/6 mice induced specific Th1 and Th17 immune responses and severe prostate inflammation and cell infiltration, mainly composed of CD4+ T cells and macrophages. In parallel, chronic pelvic pain was evidenced by increased allodynia responses. In immunized IL-17-KO mice, the presence of a prominent PAg-specific Th1 immune response that caused similar prostate inflammation and chronic pelvic pain was observed. Furthermore, markedly high PAg-specific Th1 immune responses, exacerbated prostate inflammation, and chronic pelvic pain were detected in immunized IL-4-KO mice. Conversely, immunized IL-12p40-KO mice developed PAg-specific Th2 immune responses, characterized by high IL-4 secretion, and neither infiltration nor damage in the prostate. As observed in wild type control animals, IL12p40-KO mice did not evidence tactile allodynia responses. Our results suggest that, as in patients, chronic pelvic pain is a consequence of prostate inflammation. After PA immunization, a Th1 associated immune response develops and induces prostate inflammation and chronic pelvic pain. The absence of Th1 or Th2 cytokines respectively diminishes or enhances EAP susceptibility. In addition, IL-17 showed to be dispensable for pathology induction and chronic pelvic pain development. Keywords: Prostatitis, Autoimmunity, Th1, Pain, Chronic Pelvic Pain Syndrome. Conference: IMMUNOCOLOMBIA2015 - 11th Congress of the Latin American Association of Immunology - 10o. Congreso de la Asociación Colombiana de Alergia, Asma e Inmunología, Medellin, Colombia, 13 Oct - 16 Oct, 2015. Presentation Type: Poster Presentation Topic: Autoimmunity Citation: Motrich RD, Breser ML, Sanchez LR, Godoy GJ, Prinz I and Rivero VE (2015). Th1 but not Th17 Cells are Essential for Prostate Inflammation and Chronic Pelvic Pain Development in an Experimental Model of Chronic Prostatitis/Chronic Pelvic Pain Syndrome. Front. Immunol. Conference Abstract: IMMUNOCOLOMBIA2015 - 11th Congress of the Latin American Association of Immunology - 10o. Congreso de la Asociación Colombiana de Alergia, Asma e Inmunología. doi: 10.3389/conf.fimmu.2015.05.00225 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 04 May 2015; Published Online: 14 Sep 2015. * Correspondence: PhD. Virginia E Rivero, Universidad Nacional de Cordoba, Centro de Investigaciones en Bioquímica Clínica e Inmunología (CIBICI) - Consejo Nacional de Investigaciones Cientificas y Tecnicas (CONICET), Facultad de Ciencias Químicas, Cordoba, Cordoba, 5016, Argentina, virginia.rivero@unc.edu.ar Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Ruben D Motrich Maria L Breser Leonardo R Sanchez Gloria J Godoy Immo Prinz Virginia E Rivero Google Ruben D Motrich Maria L Breser Leonardo R Sanchez Gloria J Godoy Immo Prinz Virginia E Rivero Google Scholar Ruben D Motrich Maria L Breser Leonardo R Sanchez Gloria J Godoy Immo Prinz Virginia E Rivero PubMed Ruben D Motrich Maria L Breser Leonardo R Sanchez Gloria J Godoy Immo Prinz Virginia E Rivero Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. 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