| First Author | Yadav M | Year | 2011 |
| Journal | Cell Immunol | Volume | 267 |
| Issue | 2 | Pages | 124-32 |
| PubMed ID | 21295288 | Mgi Jnum | J:168223 |
| Mgi Id | MGI:4887481 | Doi | 10.1016/j.cellimm.2011.01.001 |
| Citation | Yadav M, et al. (2011) VPAC1 (vasoactive intestinal peptide (VIP) receptor type 1) G protein-coupled receptor mediation of VIP enhancement of murine experimental colitis. Cell Immunol 267(2):124-32 |
| abstractText | Distinct roles of the two T cell G protein-coupled receptors for vasoactive intestinal peptide (VIP), termed VPAC1 and VPAC2, in VIP regulation of autoimmune diseases were investigated in the dextran sodium sulfate (DSS)-induced murine acute colitis model for human inflammatory bowel diseases. In mice lacking VPAC2 (VPAC2-KO), DSS-induced colitis appeared more rapidly with greater weight loss and severe histopathology than in wild-type mice. In contrast, DSS-induced colitis in VPAC1-KO mice was milder than in wild-type mice and VPAC2-KO mice. Tissues affected by colitis showed significantly higher levels of myeloperoxidase, IL-6, IL-1beta and MMP-9 in VPAC2-KO mice than wild-type mice, but there were no differences for IL-17, IFN-gamma, IL-4, or CCR6. Suppression of VPAC1 signals in VPAC2-KO mice by PKA inhibitors reduced the clinical and histological severity of DSS-induced colitis, as well as tissue levels of IL-6, IL-1beta and MMP-9. Thus VIP enhancement of the severity of DSS-induced colitis is mediated solely by VPAC1 receptors. |
