Copyright ©The Author(s) 2017. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Sep 7, 2017; 23(33): 6016-6029
Published online Sep 7, 2017. doi: 10.3748/wjg.v23.i33.6016
Dextran sodium sulfate colitis murine model: An indispensable tool for advancing our understanding of inflammatory bowel diseases pathogenesis
Derrick D Eichele, Kusum K Kharbanda
Derrick D Eichele, Kusum K Kharbanda, Department of Internal Medicine, Nebraska Medical Center, Omaha, NE 68198, United States
Kusum K Kharbanda, Research Service, Veterans Affairs Nebraska-Western Iowa Health Care System, Omaha, NE 68105, United States
Kusum K Kharbanda, Department of Biochemistry and Molecular Biology, Nebraska Medical Center, Omaha, NE 68198, United States
Author contributions: Both authors equally contributed to this paper with conception, literature review, drafting and critical revision, editing, and approval of the final version.
Supported by the Department of Veterans Affairs, Office of Research and Development (Biomedical Laboratory Research and Development), No. BX001155.
Conflict-of-interest statement: No potential conflicts of interest.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See:
Correspondence to: Kusum K Kharbanda, PhD, Professor, Veterans Affairs Nebraska-Western Iowa Health Care System, Research Service (151), 4101 Woolworth Avenue, Omaha, NE 68105, United States.
Telephone: +1-402-9953752 Fax: +1-402-4490604
Received: May 11, 2017
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.

Keywords: Dextran sodium sulfate, Experimental colitis, Inflammatory bowel disease, Pathogenesis, Intestinal barrier

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.