| First Author | Quick ML | Year | 2013 |
| Journal | PLoS One | Volume | 8 |
| Issue | 4 | Pages | e60987 |
| PubMed ID | 23577183 | Mgi Jnum | J:199930 |
| Mgi Id | MGI:5506651 | Doi | 10.1371/journal.pone.0060987 |
| Citation | Quick ML, et al. (2013) Th1-Th17 cells contribute to the development of uropathogenic Escherichia coli-induced chronic pelvic pain. PLoS One 8(4):e60987 |
| abstractText | The etiology of chronic prostatitis/chronic pelvic pain syndrome in men is unknown but may involve microbes and autoimmune mechanisms. We developed an infection model of chronic pelvic pain in NOD/ShiLtJ (NOD) mice with a clinical Escherichia coli isolate (CP-1) from a patient with chronic pelvic pain. We investigated pain mechanisms in NOD mice and compared it to C57BL/6 (B6) mice, a strain resistant to CP-1-induced pain. Adoptive transfer of CD4+ T cells, but not serum, from CP-1-infected NOD mice was sufficient to induce chronic pelvic pain. CD4+ T cells in CP-1-infected NOD mice expressed IFN-gamma and IL-17A but not IL-4, consistent with a Th1/Th17 immune signature. Adoptive transfer of ex-vivo expanded IFN-gamma or IL-17A-expressing cells was sufficient to induce pelvic pain in naive NOD recipients. Pelvic pain was not abolished in NOD-IFN-gamma-KO mice but was associated with an enhanced IL-17A immune response to CP1 infection. These findings demonstrate a novel role for Th1 and Th17-mediated adaptive immune mechanisms in chronic pelvic pain. |
