Published online Sep 7, 2017. doi: 10.3748/wjg.v23.i33.6016
Peer-review started: May 12, 2017
First decision: June 5, 2017
Revised: July 7, 2017
Accepted: August 1, 2017
Article in press: August 2, 2017
Published online: September 7, 2017
Inflammatory bowel diseases (IBD), including Crohn’s disease and ulcerative colitis, are complex diseases that result from the chronic dysregulated immune response in the gastrointestinal tract. The exact etiology is not fully understood, but it is accepted that it occurs when an inappropriate aggressive inflammatory response in a genetically susceptible host due to inciting environmental factors occurs. To investigate the pathogenesis and etiology of human IBD, various animal models of IBD have been developed that provided indispensable insights into the histopathological and morphological changes as well as factors associated with the pathogenesis of IBD and evaluation of therapeutic options in the last few decades. The most widely used experimental model employs dextran sodium sulfate (DSS) to induce epithelial damage. The DSS colitis model in IBD research has advantages over other various chemically induced experimental models due to its rapidity, simplicity, reproducibility and controllability. In this manuscript, we review the newer publicized advances of research in murine colitis models that focus upon the disruption of the barrier function of the intestine, effects of mucin on the development of colitis, alterations found in microbial balance and resultant changes in the metabolome specifically in the DSS colitis murine model and its relation to the pathogenesis of IBD.
Core tip: In the last few decades the proliferation of research in experimental colitis models of inflammatory bowel diseases (IBD) has had profound effects in our understanding of human IBD pathophysiology as well as to exploit potential therapeutic avenues outside of immunologic therapy. The dextran sodium sulfate colitis model, through its rapidity, simplicity, reproducibility and controllability has been instrumental in our understanding of intestinal barrier function through the dysregulation of mucin, interaction with the intestinal microbiome and metabolome.