Comparison of experimental mouse models of inflammatory bowel disease

  • Authors:
    • Soo Youn Oh
    • Kyung-Ah Cho
    • Jihee Lee Kang
    • Kwang Ho Kim
    • So-Youn Woo
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  • Published online on: November 27, 2013     https://doi.org/10.3892/ijmm.2013.1569
  • Pages: 333-340
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Abstract

Inflammatory bowel disease (IBD) is multifactorial and involves immunological, environmental and genetic factors. Although there are no animal models that effectively mimic human IBD, experimental models allow us to analyze the mechanisms of chronic intestinal inflammation. IBD can be induced in mice by dextran sulfate sodium (DSS) or by a 2,4,6-trinitrobenzene sulfonic acid (TNBS)‑ethanol enema, which evoke immune responses and colitis. In this study, in order to compare the mechanisms of inflammatory response in mice, 3 distinct models of IBD were established: 2% TNBS-induced acute colitis, 4% DSS-induced acute colitis and 2% DSS-induced chronic colitis. In addition, to evaluate the effects of TNBS on inflammasome activation, we used caspase-1 knockout (KO) mice. Changes in both body weight and survival became prominent after day 1 in the 2% TNBS‑induced colitis model, and after day 5 in the 4% DSS-induced colitis model. The TNBS- and DSS-treated mice, but not the caspase-1 KO mice, showed a massive bowel edema and disruption of epithelial cells. The level of CD11b+Gr-1+ myeloid-derived suppressor cells (MDSCs) was increased in all tested tissues of the TNBS- and DSS-treated groups, apart from the basal membrane (BM) in the DSS-induced colitis groups and the lamina propria (LP) in the DSS-induced chronic colitis group. We further analyzed different subsets of CD4+ T cells in LP and found that the levels of interferon (IFN)γ‑secreting (IFNγ+), IL-17‑secreting (IL-17+), but not those of IL-4-secreting (IL-4+) T cells increased upon treatment with TNBS or DSS. In addition, discrepancies between the histopathologies of wild-type and caspase-1 KO mice indicated that the pathogenesis of IBD may be associated with the inflammasome pathway responses mediated by caspase‑1 in TNBS‑induced colitis.
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2014-February
Volume 33 Issue 2

Print ISSN: 1107-3756
Online ISSN:1791-244X

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Spandidos Publications style
Oh SY, Cho K, Kang JL, Kim KH and Woo S: Comparison of experimental mouse models of inflammatory bowel disease. Int J Mol Med 33: 333-340, 2014
APA
Oh, S.Y., Cho, K., Kang, J.L., Kim, K.H., & Woo, S. (2014). Comparison of experimental mouse models of inflammatory bowel disease. International Journal of Molecular Medicine, 33, 333-340. https://doi.org/10.3892/ijmm.2013.1569
MLA
Oh, S. Y., Cho, K., Kang, J. L., Kim, K. H., Woo, S."Comparison of experimental mouse models of inflammatory bowel disease". International Journal of Molecular Medicine 33.2 (2014): 333-340.
Chicago
Oh, S. Y., Cho, K., Kang, J. L., Kim, K. H., Woo, S."Comparison of experimental mouse models of inflammatory bowel disease". International Journal of Molecular Medicine 33, no. 2 (2014): 333-340. https://doi.org/10.3892/ijmm.2013.1569