Dextran Sulfate Sodium (DSS)‐Induced Colitis in Mice

Abstract

Inflammatory bowel diseases (IBD) mainly comprised of Ulcerative Colitis and Crohn's Disease are complex and multifactorial disease with unknown etiology. For the past 20 years, to study human IBD mechanistically, number of murine models of colitis has been developed. These models are indispensable tools to decipher underlying mechanisms of IBD pathogenesis as well as to evaluate number potential therapeutics. Among various chemical induced colitis models, DSS-induced colitis model is widely used because of its simplicity and many similarities with human ulcerative colitis. This model has both advantages and disadvantages that need to be considered when employed. The current protocol aimed to extensively describe the DSS-induced colitis model, focusing on its detailed protocol as well as factors that could affect DSS-induced pathology.

Streptococcus thermophilus NCIMB 41856 ameliorates signs of colitis in an animal model of inflammatory bowel disease

“…However, it is not a perfect model and the mechanism by which it induces inflammation is not entirely understood. It is thought that inflammation results from damage to the epithelial cells lining the colon which allows dissemination of pro-inflammatory intestinal contents into the tissue (Chassaing et al, 2014). In this study, animals were being treated with DSS for the duration of the experiment; it was a progressive model with a continuous chemical assault on the epithelial cells lining the gut, therefore, a cure of colitis by S. thermophilus would not be expected.…”

Intestinal myofibroblast-specific Tpl2-Cox-2-PGE 2 pathway links innate sensing to epithelial homeostasis

“…This discrepancy could result from the different genetic background used or from experimental conditions such as the use of littermate and cohoused mice; the DSS model is particularly sensitive to these factors because the intestinal microflora is shaped through maternal transfer in a long-term manner (40) bearing transferrable colitogenic activity in the DSS model (41). To avoid microflora and genetic confounding, in the present study we performed our experiments using only large groups of littermate and cohoused mice as recommended (42,43), which was not clarified in the study by Lawrenz et al (39). In addition, Tpl2 inhibitor administration in DSS-treated C57BL/6 WT mice did not confer protection, compared with cohoused littermate controls, in contrast to the result reported by Lawrenz et al for the same dosage (39) (SI Appendix, Fig.…”

The transcriptional repressor HIC1 regulates intestinal immune homeostasis

“…This model involves chemically induced epithelial cell damage, which leads to bacterial translocation and activation of sub-epithelial innate immune cells and therefore does not require T or B cells for development of disease. 34,35 Hic1 fl/fl mice and Hic1 DT mice were exposed to 3.5% DSS in their drinking water for 7 days before returning to regular drinking water for one final day. DSS-treated Hic1 DT mice exhibited attenuated weight loss in comparison with treated Hic1 fl/fl mice (Supplementary Figure 6a).…”