tryptasepar2 axis in experimental autoimmune prostatitis a model for chronic pelvic pain syndrome chronic prostatitischronic pelvic pain syndrome cpcpps affects up to 15 of the male population and is characterized by pelvic pain mast cells are implicated in the murine experimental autoimmune prostatitis eap model as key to chronic pelvic pain development the mast cell mediator tryptase and its cognate receptor proteaseactivated receptor 2 par2 are involved in mediating pain in other visceral disease models prostatic secretions and urines from cpcpps patients were examined for the presence of mast cell degranulation products tryptase and par2 expression were examined in murine eap pelvic pain and inflammation were assessed in the presence or absence of par2 expression and upon par2 neutralization tryptase and carboxypeptidase a3 were elevated in cpcpps compared to healthy volunteers tryptase was capable of inducing pelvic pain and was increased in eap along with its receptor par2 par2 was required for the development of chronic pelvic pain in eap par2 signaling in dorsal root ganglia led to extracellular signalregulated kinase erk12 phosphorylation and calcium influx par2 neutralization using antibodies attenuated chronic pelvic pain in eap the tryptasepar2 axis is an important mediator of pelvic pain in eap and may play a role in the pathogenesis of cpcpps