IL-17 is not essential for inflammation and chronic pelvic pain development in an experimental model of chronic prostatitis/chronic pelvic pain syndrome.

MOTRICH RD; BRESER ML; SANCHEZ JG; GODOY GJ; RIVERO VE

PAIN

ELSEVIER SCIENCE BV

Lugar: Amsterdam; Año: 2017 vol. 157 p. 585 - 585

0304-3959

ain and inflammation in the absence of infection are hallmarks in chronic prostatitis and 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 paindevelopment in EAP using IL-12p40-KO, IL-4-KO, IL-17-KO, and wild-type (C57BL/6) mice. Prostate antigen (PAg) immunization inC57BL/6 mice induced specific Th1 and Th17 immune responses and severe prostate inflammation and cell infiltration, mainlycomposed of CD41 T cells and macrophages. Moreover, chronic pelvic pain was evidenced by increased allodynia responses. Inimmunized IL-17-KOmice, the presence of a prominent PAg-specific Th1 immune response caused similar prostate inflammation andchronic pelvic pain. Furthermore,markedly high PAg-specific Th1 immune responses, exacerbated prostate inflammation, and