info:eu-repo/semantics/article
IL-17 is not essential for prostate inflammation and chronic pelvic pain development in an experimental model of chronic prostatitis/chronic pelvic pain syndrome
Date
2015-11Registration in:
Motrich, Ruben Dario; Breser, Maria Laura; Sanchez, Leonardo Rodolfo; Godoy, Gloria Janet; Prinz, Immo; et al.; IL-17 is not essential for prostate inflammation and chronic pelvic pain development in an experimental model of chronic prostatitis/chronic pelvic pain syndrome; Elsevier Science; Pain; 157; 3; 11-2015; 585-597
0304-3959
1872-6623
CONICET Digital
CONICET
Author
Motrich, Ruben Dario
Breser, Maria Laura
Sanchez, Leonardo Rodolfo
Godoy, Gloria Janet
Prinz, Immo
Rivero, Virginia Elena
Abstract
Pain and inflammation in the absence of infection are hallmarks in Chronic Prostatitis/Chronic Pelvic Pain Syndrome (CP/CPPS) patients. The etiology of CP/CPPS is unclear and autoimmunity has been proposed as a cause. Experimental Autoimmune Prostatitis (EAP) models have long been used for studying CP/CPPS. Herein, we studied prostate inflammation induction and chronic pelvic pain development in EAP using IL-12p40-KO, IL-4-KO, IL-17-KO, and wild type (C57BL/6) mice. Prostate antigen (PAg)-immunization in 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. Moreover, 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 caused similar prostate inflammation and chronic pelvic pain. 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 PAg 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 not to be essential for pathology induction and chronic pelvic pain development.
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