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Dextran Sodium Sulfate Colitis Murine Model: An Indispensable Tool for Advancing Our Understanding of Inflammatory Bowel Diseases Pathogenesis

Overview
Specialty Gastroenterology
Date 2017 Oct 4
PMID 28970718
Citations 336
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Abstract

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.

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References
1.
Grill J, Neumann J, Hiltwein F, Kolligs F, Schneider M . Intestinal E-cadherin Deficiency Aggravates Dextran Sodium Sulfate-Induced Colitis. Dig Dis Sci. 2015; 60(4):895-902. DOI: 10.1007/s10620-015-3551-x. View

2.
Hoebler C, Gaudier E, de Coppet P, Rival M, Cherbut C . MUC genes are differently expressed during onset and maintenance of inflammation in dextran sodium sulfate-treated mice. Dig Dis Sci. 2006; 51(2):381-9. DOI: 10.1007/s10620-006-3142-y. View

3.
Randhawa P, Singh K, Singh N, Jaggi A . A review on chemical-induced inflammatory bowel disease models in rodents. Korean J Physiol Pharmacol. 2014; 18(4):279-88. PMC: 4146629. DOI: 10.4196/kjpp.2014.18.4.279. View

4.
Gong Y, Li H, Li Y . Effects of Bacillus subtilis on Epithelial Tight Junctions of Mice with Inflammatory Bowel Disease. J Interferon Cytokine Res. 2016; 36(2):75-85. DOI: 10.1089/jir.2015.0030. View

5.
Poritz L, Garver K, Green C, Fitzpatrick L, Ruggiero F, Koltun W . Loss of the tight junction protein ZO-1 in dextran sulfate sodium induced colitis. J Surg Res. 2007; 140(1):12-9. DOI: 10.1016/j.jss.2006.07.050. View