4.4 Article

Overexpression of GATA-3 in T Cells Accelerates Dextran Sulfate Sodium-Induced Colitis

Journal

EXPERIMENTAL ANIMALS
Volume 63, Issue 2, Pages 133-140

Publisher

INT PRESS EDITING CENTRE INC
DOI: 10.1538/expanim.63.133

Keywords

dextran sulfate sodium; GATA-3; IL-13; inflammatory bowel disease; T helper cell

Funding

  1. JSPS KAKENHI [24650228]
  2. KAKENHI [25461240]
  3. Grants-in-Aid for Scientific Research [24650228, 25461240] Funding Source: KAKEN

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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 (RORyt 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.

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