Experimental Models of Inflammatory Bowel Diseases
By P. Kiesler, I. Fuss, W. Strober. Cellular and Molecular Gastroenterology and Hepatology, 2015
617 citations recorded by the source corpus.
The understanding of the intestinal inflammation occurring in the inflammatory bowel diseases (IBD) has been immeasurably advanced by the development of the now numerous murine models of intestinal inflammation. The usefulness of this research tool in IBD studies has been enabled by our improved knowledge of mucosal immunity and thus our improved ability to interpret the complex responses of mice with various causes of colitis; in addition, it has been powered by the availability of models in which the mice have specific genetic and/or immunologic defects that can be related to the origin of the inflammation. Finally, and more recently, it has been enhanced by our newly acquired ability to define the intestinal microbiome under various conditions and thus to understand how intestinal microorganisms impact on inflammation. In this brief review of murine models of intestinal inflammation we focus mainly on the most often used models that are, not incidentally, also the models that have yielded major insights into IBD pathogenesis.
Subfields: Genetics, Molecular Biology, Surgery
View Paper: https://www.semanticscholar.org/paper/39a4a5ce64cdd83305aa92adb249530f27319376
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Citations in the corpus
- Cytokine Networks in the Pathophysiology of Inflammatory Bowel Disease. (2019, background): “…in mouse models that offer unique opportunities to dissect the dynamics of cytokine regulation and establish causal functional links to support the development of cytokine-targeted therapies in IBD (Table 1, for specifics of the discussed mouse models, please refer to (Kiesler et al., 2015)).”
- Cell Biology of Tight Junction Barrier Regulation and Mucosal Disease (2018, background): “It is therefore not surprising that almost any substantial defect in mucosal immune regulation results in enterocolitis in experimental animals and humans (Kuhn et al. 1993; Powrie et al. 1994; d’Hennezel et al. 2009; Glocker et al. 2009; Hayes et al. 2015; Kiesler et al. 2015; Mishima et al. 2015).”