Dextran Sulfate Sodium (DSS)-induced ulcerative colitis model in mice: comparing the effects of two therapies on clinical signs and colon cytokines secretion
Inflammatory bowel disease (IBD), which is a chronic inflammatory condition of the gastrointestinal tract, affects millions of people world-wide. Although the exact etiology of the disease is unknown, research works suggest that IBD might be caused by microbiome dysbiosis as well as environmental and genetic factors. Common symptoms of IBD include abdominal pain, presence of occult or visible blood in stool, diarrhea and weight loss. IBD can drastically decrease quality of life and, if kept untreated for long, it can lead to other major complications including colon cancer. Current, anti-IBD treatment options are also suboptimal, and thus researchers are actively looking for better and more efficacious therapies for IBD.
As with most human diseases, animal models are often created to mimic IBD conditions to understand the disease mechanisms as well as to explore efficacy of novel anti-IBD agents. Among the various animal models that are used to mimic human IBD, the dextran sulfate sodium (DSS)-induced colitis model in mice is more widely used due to its simplicity and recapitulation of several features observed in human ulcerative colitis. In this model, DSS is provided ad libitum in drinking water to induce the disease. However, reproducibility of data is often the biggest challenge in the mouse DSS model. Animal strain, source and sex, molecular weight of DSS, DSS concentration and protocol to induce the disease often need to be streamlined to consistently induce the model in mice. In the present study, we identified an optimal DSS concentration and protocol for disease induction. Afterwards, we compared the efficacy of two anti-IBD therapies, Cyclosporine A and 5-Amino Salicylic Acid in the model. Our results suggest that the mouse DSS colitis model is more responsive to Cyclosporine A treatment and this agent can be used as a positive control for the model.