Dextran sodium sulfate colitis murine model: An indispensable tool for advancing our understanding of inflammatory bowel diseases pathogenesis
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 aggressiv...
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| Published in | World journal of gastroenterology : WJG Vol. 23; no. 33; pp. 6016 - 6029 |
|---|---|
| Main Authors | , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Baishideng Publishing Group Inc
07.09.2017
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| Subjects | |
| Online Access | Get full text |
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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 respon-se in a genetically susceptible host due to inciting environmental factors occurs. To investigate the path-ogenesis 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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| AbstractList | 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 respon-se in a genetically susceptible host due to inciting environmental factors occurs. To investigate the path-ogenesis 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. 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.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. 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. |
| Author | Derrick D Eichele Kusum K Kharbanda |
| AuthorAffiliation | Department of Internal Medicine,Nebraska Medical Center;Research Service,Veterans Affairs Nebraska-Western Iowa Health Care System;Department of Biochemistry and Molecular Biology,Nebraska Medical Center |
| Author_xml | – sequence: 1 givenname: Derrick D surname: Eichele fullname: Eichele, Derrick D – sequence: 2 givenname: Kusum K surname: Kharbanda fullname: Kharbanda, Kusum K |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/28970718$$D View this record in MEDLINE/PubMed |
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| Keywords | Inflammatory bowel disease Experimental colitis Intestinal barrier Dextran sodium sulfate Pathogenesis |
| Language | English |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 ObjectType-Review-3 content type line 23 Telephone: +1-402-9953752 Fax: +1-402-4490604 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. kkharbanda@unmc.edu 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. |
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| Snippet | Inflammatory bowel diseases(IBD),including Crohn’s disease and ulcerative colitis,are complex diseases that result from the chronic dysregulated immune... Inflammatory bowel diseases (IBD), including Crohn's disease and ulcerative colitis, are complex diseases that result from the chronic dysregulated immune... Inflammatory bowel diseases (IBD), including Crohn’s disease and ulcerative colitis, are complex diseases that result from the chronic dysregulated immune... |
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| SubjectTerms | Animals Colon - metabolism Colon - pathology Cytokines - metabolism Dextran Sulfate - toxicity Disease Models, Animal Gastrointestinal Microbiome - immunology Humans Inflammatory Bowel Diseases - chemically induced Inflammatory Bowel Diseases - drug therapy Inflammatory Bowel Diseases - etiology Inflammatory Bowel Diseases - pathology Metabolome Mice Mucins - metabolism Permeability Probiotics - therapeutic use Reproducibility of Results Review Time Factors |
| Title | Dextran sodium sulfate colitis murine model: An indispensable tool for advancing our understanding of inflammatory bowel diseases pathogenesis |
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