Here is a good review article on the topic. DSS or TNBS are the big two and are discussed here.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4146629/
Many colitis models in mice exist: spontaneous, chemically-induced, and T cell-transfer models. Each one has its particular features, and you gotta find which one suit you best, depending on the aim of your research.
The spontaneous models of colitis are genetic-driven. For example, IL10-knockout mice (il10-/-) develop wasting disease and colitis without any additional treatment (Kuhn R, Lohler J, Rennick D, et al. Interleukin-10-deficient mice develop chronic enterocolitis. Cell 1993;75:263–274), it's a broadly used model.
Chemically-induced models are several, and can be used in diverse ways. 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis presents Crohn-like histological and immunological (TH1/TH17) features, while oxalozone-induced colitis it’s a Ulcerative Colitis-like model (with marked TH2/TH9 bias). Both models are technically performed the same: intra-rectal administration of the chemical dissolved in ethanol, with or without skin presensitization. Although the usual way to use these models is by a single intra-rectal administration, at least for the TNBS model it can be achieved a chronic type of inflammation through two or more intra-rectal administrations, giving lesser doses (it can be used to study fibrosis also).
Dextran sulfate sodium (DSS)-induced intestinal inflammation it’s widely used, not only as a colitis model but also to study wound healing of the intestinal epithelium. DSS is administered in the drinking water and depending on the concentration and the frequency of administration, acute, chronic and/or relapsing models of colitis can be achieved. Despite it has being shown that the DSS-colitis is mediated mainly by neutrophils, TH2-derived cytokines are also involved in the inflammatory response (IL4, IL13).
All chemical-induced models of colitis are strain, microbiota and genre-dependent (females are resistant to TNBS, for example). So, you have to optimize your model of intestinal inflammation with the particular strain of mice you have, and the facilities with which you count. You can find basic protocols of chemical-induced colitis in Wirtz S, Neufert C, Weigmann B & Neurath MF. Chemically induced mouse models of intestinal inflammation. Nature Protocols 2007; 2:541–546.
Lastly, there’s the T-cell transfer model of colitis. In this model, intestinal inflammation is achieved by adoptive transfer of CD4+CD25-CD45RBhigh cells in immunodeficient mice: Rag1-/- or Rag2-/-. There are some works in Nude and SCID mice, but they are controversial due to the possibility of thymus-independent T-cell differentiation in gut. Overall, the T-cell transfer model of colitis renders a chronic TH1-type of inflammation (assessed 4-8 weeks post T-cell transfer), with high levels of IFNg-producing T-cells in lamina propria of colon. It’s a broadly used, but you have to count with a FACS. Here’s a nice protocol: Steinbach EC, Gipson GR, Sheikh SZ. Induction of Murine Intestinal Inflammation by Adoptive Transfer of Effector CD4+CD45RBhigh T Cells into Immunodeficient Mice. J Vis Exp. 2015;21;(98). doi: 10.3791/52533.
I hope it helps you.
Good luck!
Luciano.
- Badges
- Science topic