{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,10]],"date-time":"2026-06-10T00:15:14Z","timestamp":1781050514032,"version":"3.54.1"},"reference-count":32,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Regulatory, Integrative and Comparative Physiology"],"published-print":{"date-parts":[[2012,9,15]]},"abstract":"<jats:p>Experimental autoimmune prostatitis (EAP) is a murine model of chronic prostatitis\/chronic pelvic pain syndrome (CPPS) in men, a syndrome characterized by chronic pelvic pain. We have demonstrated that chemokine ligands CCL2 and CCL3 are biomarkers that correlate with pelvic pain symptoms. We postulated that CCL2 and CCL3 play a functional role in CPPS and therefore examined their expression in EAP. Upon examination of the prostate 5 days after induction of EAP, CCL2 mRNA was elevated 2- to 3-fold, CCL8 by 15-fold, CCL12 by 12- to 13-fold, and CXCL9 by 2- to 4-fold compared with control mice. At 10 days the major chemokines were CXCL13 and CXCL2; at 20 days CCL2 (1- to 2-fold), CCL3 (2- to 3-fold) and CCL11 (2- to 3-fold); and at 30 days, CCL12 (20- to 35-fold) and smaller increases in CCL2, CCL3, and XCL1. Chemokine elevations were accompanied by increases in mast cells and B cells at 5 days, monocytes and neutrophils at day 10, CD4+ T cells at day 20, and CD4+ and CD8+ T cells at day 30. Anti-CCL2 and anti-CCL3 neutralizing antibodies administered at EAP onset attenuated pelvic pain development, but only anti-CCL2 antibodies were effective therapeutically. CCL2- and its cognate receptor CCR2-deficient mice were completely protected from development of pain symptoms but assumed susceptibility after reconstitution with wild-type bone marrow. CCL3-deficient mice showed resistance to the maintenance of pelvic pain while CCR5-deficient mice did not show any lessening of pelvic pain severity. These results suggest that the CCL2-CCR2 axis and CCL3 are important mediators of chronic pelvic pain in EAP.<\/jats:p>","DOI":"10.1152\/ajpregu.00240.2012","type":"journal-article","created":{"date-parts":[[2012,7,20]],"date-time":"2012-07-20T09:49:05Z","timestamp":1342777745000},"page":"R580-R589","source":"Crossref","is-referenced-by-count":70,"title":["CCL2 and CCL3 are essential mediators of pelvic pain in experimental autoimmune prostatitis"],"prefix":"10.1152","volume":"303","author":[{"given":"Marsha L.","family":"Quick","sequence":"first","affiliation":[{"name":"Departments of Urology,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Soumi","family":"Mukherjee","sequence":"additional","affiliation":[{"name":"Departments of Urology,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Charles N.","family":"Rudick","sequence":"additional","affiliation":[{"name":"Departments of 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