| First Author | Okamura M | Year | 2014 |
| Journal | Exp Anim | Volume | 63 |
| Issue | 2 | Pages | 133-40 |
| PubMed ID | 24770638 | Mgi Jnum | J:312629 |
| Mgi Id | MGI:6791947 | Doi | 10.1538/expanim.63.133 |
| Citation | Okamura M, et al. (2014) Overexpression of GATA-3 in T cells accelerates dextran sulfate sodium-induced colitis. Exp Anim 63(2):133-40 |
| abstractText | Ulcerative colitis (UC) is an inflammatory bowel disease, and its pathogenesis includes genetic, environmental, and immunological factors, such as T helper cells and their secreted cytokines. T helper cells are classified as Th1, Th2, and Th17 cells. However, it is unclear which T helper cells are important in UC. Dextran sulfate sodium (DSS)-induced colitis is a commonly used model of UC. In this study, we induced DSS colitis in Th1 dominant (T-bet transgenic (Tg)) mice, Th2 dominant (GATA-3 Tg) mice, and Th17 dominant (RORgammat Tg) mice to elucidate the roles of T helper cell in DSS colitis. The results showed that GATA-3 Tg mice developed the most severe DSS colitis compared with the other groups. GATA-3 Tg mice showed a significant decreased in weight from day 1 to day 7, and an increased high score for the disease activity index compared with the other groups. Furthermore, GATA-3 Tg mice developed many ulcers in the colon, and many neutrophils and macrophages were detected on day 4 after DSS treatment. Measurement of GATA-3-induced cytokines demonstrated that IL-13 was highly expressed in the colon from DSS-induced GATA-3 Tg mice. In conclusion, GATA-3 overexpression in T-cells and IL-13 might play important roles in the development of DSS colitis. |
