Dextran sodium sulfate colitis murine model

An indispensable tool for advancing our understanding of inflammatory bowel diseases pathogenesis

Derrick D. Eichele, Kusum Kharbanda

Research output: Contribution to journalReview article

41 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)6016-6029
Number of pages14
JournalWorld Journal of Gastroenterology
Volume23
Issue number33
DOIs
StatePublished - Sep 7 2017
Externally publishedYes

Fingerprint

Dextran Sulfate
Colitis
Inflammatory Bowel Diseases
Theoretical Models
Metabolome
Mucins
Ulcerative Colitis
Research
Crohn Disease
Intestines
Gastrointestinal Tract
Chronic Disease
Animal Models

Keywords

  • Dextran sodium sulfate
  • Experimental colitis
  • Inflammatory bowel disease
  • Intestinal barrier
  • Pathogenesis

ASJC Scopus subject areas

  • Gastroenterology

Cite this

Dextran sodium sulfate colitis murine model : An indispensable tool for advancing our understanding of inflammatory bowel diseases pathogenesis. / Eichele, Derrick D.; Kharbanda, Kusum.

In: World Journal of Gastroenterology, Vol. 23, No. 33, 07.09.2017, p. 6016-6029.

Research output: Contribution to journalReview article

@article{6717277f0b03421690b297ba6aa0ec2d,
title = "Dextran sodium sulfate colitis murine model: An indispensable tool for advancing our understanding of inflammatory bowel diseases pathogenesis",
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.",
keywords = "Dextran sodium sulfate, Experimental colitis, Inflammatory bowel disease, Intestinal barrier, Pathogenesis",
author = "Eichele, {Derrick D.} and Kusum Kharbanda",
year = "2017",
month = "9",
day = "7",
doi = "10.3748/wjg.v23.i33.6016",
language = "English (US)",
volume = "23",
pages = "6016--6029",
journal = "World Journal of Gastroenterology",
issn = "1007-9327",
publisher = "WJG Press",
number = "33",

}

TY - JOUR

T1 - Dextran sodium sulfate colitis murine model

T2 - An indispensable tool for advancing our understanding of inflammatory bowel diseases pathogenesis

AU - Eichele, Derrick D.

AU - Kharbanda, Kusum

PY - 2017/9/7

Y1 - 2017/9/7

N2 - 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.

AB - 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.

KW - Dextran sodium sulfate

KW - Experimental colitis

KW - Inflammatory bowel disease

KW - Intestinal barrier

KW - Pathogenesis

UR - http://www.scopus.com/inward/record.url?scp=85029187760&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85029187760&partnerID=8YFLogxK

U2 - 10.3748/wjg.v23.i33.6016

DO - 10.3748/wjg.v23.i33.6016

M3 - Review article

VL - 23

SP - 6016

EP - 6029

JO - World Journal of Gastroenterology

JF - World Journal of Gastroenterology

SN - 1007-9327

IS - 33

ER -