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      Dextran Sulfate Sodium (DSS)‐Induced Colitis in Mice

      Author(s): 1 , 1 , 1 , 2 , 3
      Publication date Created:
      Publication date (Electronic):
      Journal: Current Protocols in Immunology
      Publisher: Wiley

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          Abstract

          Inflammatory bowel diseases (IBD), mainly comprising ulcerative colitis and Crohn's Disease, are complex and multifactorial diseases with unknown etiology. For the past 20 years, to study human IBD mechanistically, a number of murine models of colitis have been developed. These models are indispensable tools to decipher underlying mechanisms of IBD pathogenesis as well as to evaluate a number of potential therapeutics. Among various chemically induced colitis models, the dextran sulfate sodium (DSS)-induced colitis model is widely used because of its simplicity and many similarities with human ulcerative colitis. This model has both advantages and disadvantages that must be considered when employed. This protocol describes the DSS-induced colitis model, focusing on details and factors that could affect DSS-induced pathology.

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          Recognition of commensal microflora by toll-like receptors is required for intestinal homeostasis.

          Seth Rakoff-Nahoum, Justin Paglino, Fatima Eslami-Varzaneh … (2004)
          Toll-like receptors (TLRs) play a crucial role in host defense against microbial infection. The microbial ligands recognized by TLRs are not unique to pathogens, however, and are produced by both pathogenic and commensal microorganisms. It is thought that an inflammatory response to commensal bacteria is avoided due to sequestration of microflora by surface epithelia. Here, we show that commensal bacteria are recognized by TLRs under normal steady-state conditions, and this interaction plays a crucial role in the maintenance of intestinal epithelial homeostasis. Furthermore, we find that activation of TLRs by commensal microflora is critical for the protection against gut injury and associated mortality. These findings reveal a novel function of TLRs-control of intestinal epithelial homeostasis and protection from injury-and provide a new perspective on the evolution of host-microbial interactions.
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            The commensal microbiota and enteropathogens in the pathogenesis of inflammatory bowel diseases.

            Benoit Chassaing, Arlette Darfeuille-Michaud (2011)
            Intestinal inflammation arises from abnormal host-microbe interactions. The perturbations of homeostatic coexistence involve host genetic factors, barrier function, innate and adaptive immunity, as well as qualitative and quantitative changes in the composition of the microbiota. Dysbiosis toward selected micro-organisms and decreased complexity of commensal bacteria have been observed in patients with Crohn's disease and ulcerative colitis, but it is not clear whether the dysbiosis contributes to development of inflammatory bowel disease or is instead a consequence of the disease. Pathogens with virulence factors that allow them to breach the intestinal barrier and induce chronic inflammation might mediate the pathogenesis of these diseases. To identify new therapeutic approaches for inflammatory bowel disease, it is important to identify host susceptibility factors involved in the control of microbial infection, characterize potential pathogens, and eliminate them or block the expression of their virulence factors. Copyright © 2011 AGA Institute. Published by Elsevier Inc. All rights reserved.
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              Loss of the tight junction protein ZO-1 in dextran sulfate sodium induced colitis.

              Lisa S. Poritz, Kristian I. Garver, Cecelia Green … (2007)
              Inflammatory bowel disease (IBD) is associated with increased intestinal permeability and decreased expression of tight junction (TJ) proteins in the inflamed mucosa. Whether this alteration in TJ expression is a prerequisite for the development of intestinal inflammation or a secondary result of that inflammation is unknown. This study looked at the expression of the TJ protein ZO-1 and the corresponding permeability changes in dextran sulfate sodium (DSS) induced colitis in a mouse model. BALB/c mice were fed 3% DSS or water for 1, 3, 5, or 7 days. The animals were weighed, stool was checked for blood, and the colon length measured. Segments of the colon were used for histology, immunohistochemistry for ZO-1, or Western blot for TJ proteins. Colonic permeability was measured using Evan's Blue dye. DSS treated animals had heme positive stools, colitis by histology, significant weight loss, and colon shortening. There was an absence of ZO-1 by Western blot in the 7-day DSS treated animals, double the amount of claudin-1 and normal cytokeratin. The loss of ZO-1 started after 1 d of DSS treatment and was followed by a significant increase in permeability to Evan's blue by day 3. The loss of ZO-1 and increased permeability preceded the development of significant intestinal inflammation suggesting that in DSS colitis alterations in the TJ complex occur before the intestinal inflammation and not as a consequence of it. These changes in the TJ complex may facilitate the development of the inflammatory infiltrate seen in colitis.
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                Author and article information

                Journal
                Title: Current Protocols in Immunology
                Abbreviated Title: Current Protocols in Immunology
                Publisher: Wiley
                ISSN (Print): 1934-3671
                ISSN (Electronic): 1934-368X
                Publication date Created: February 04 2014
                Publication date Created: February 2014
                Publication date (Electronic): February 04 2014
                Publication date (Print): February 2014
                Volume: 104
                Issue: 1
                Affiliations
                [1 ]Center for Inflammation, Immunity, & Infection, Department of Biology, Georgia State University Atlanta Georgia
                [2 ]Department of Nutritional Sciences, The Pennsylvania State University University Park Pennsylvania
                [3 ]Department of Medicine, The Pennsylvania State University College of Medicine Hershey Pennsylvania
                Article
                DOI: 10.1002/0471142735.im1525s104
                PMC ID: 3980572
                PubMed ID: 24510619
                SO-VID: 6616a925-1eae-4e7f-ba56-0d2488270910
                Copyright © © 2014
                License:

                http://onlinelibrary.wiley.com/termsAndConditions#vor

                http://doi.wiley.com/10.1002/tdm_license_1.1

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