| First Author | Matsuo Y | Year | 2015 |
| Journal | Int Immunopharmacol | Volume | 29 |
| Issue | 2 | Pages | 468-475 |
| PubMed ID | 26476684 | Mgi Jnum | J:342819 |
| Mgi Id | MGI:7550470 | Doi | 10.1016/j.intimp.2015.10.011 |
| Citation | Matsuo Y, et al. (2015) Interleukin 19 reduces inflammation in chemically induced experimental colitis. Int Immunopharmacol 29(2):468-475 |
| abstractText | Inflammatory bowel disease results from chronic dysregulation of the mucosal immune system and aberrant activation of both the innate and adaptive immune responses. Interleukin (IL)-19, a member of the IL-10 family, functions as an anti-inflammatory cytokine. Here, we investigated the contribution of IL-19 to intestinal inflammation in a model of T cell-mediated colitis in mice. Inflammatory responses in IL-19-deficient mice were assessed using the 2,4,6-trinitrobenzene sulfonic acid (TNBS) model of acute colitis. IL-19 deficiency aggravated TNBS-induced colitis and compromised intestinal recovery in mice. Additionally, the exacerbation of TNBS-induced colonic inflammation following genetic ablation of IL-19 was accompanied by increased production of interferon-gamma, IL-12 (p40), IL-17, IL-22, and IL-33, and decreased production of IL-4. Moreover, the exacerbation of colitis following IL-19 knockout was also accompanied by increased production of CXCL1, G-CSF and CCL5. Using this model of induced colitis, our results revealed the immunopathological relevance of IL-19 as an anti-inflammatory cytokine in intestinal inflammation in mice. |
