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Worms, flies and four-legged friends: the applicability of biological models to the understanding of intestinal inflammatory diseases

Diseases of intestinal inflammation, including Crohn’s disease, ulcerative colitis and necrotizing enterocolitis, cause substantial acute and chronic disability in a large proportion of the population. Crohn’s disease and ulcerative colitis, which are collectively referred to as inflammatory bowel d...

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Autores principales: Lin, Joyce, Hackam, David J.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Company of Biologists Limited 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3124049/
https://www.ncbi.nlm.nih.gov/pubmed/21669933
http://dx.doi.org/10.1242/dmm.007252
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author Lin, Joyce
Hackam, David J.
author_facet Lin, Joyce
Hackam, David J.
author_sort Lin, Joyce
collection PubMed
description Diseases of intestinal inflammation, including Crohn’s disease, ulcerative colitis and necrotizing enterocolitis, cause substantial acute and chronic disability in a large proportion of the population. Crohn’s disease and ulcerative colitis, which are collectively referred to as inflammatory bowel disease (IBD), lead to recurrent episodes of intestinal dysfunction and systemic illness, whereas necrotizing enterocolitis is characterized by the development of dramatic and all too often fatal intestinal necrosis in infants. To determine the molecular underpinnings of these disorders, investigators have explored a variety of animal models that vary widely in their complexity. These experimental systems include the invertebrate nematode Caenorhabditis elegans, the more complex invertebrate Drosophila melanogaster, and vertebrate systems including mice, rats and other mammals. This review explores the experimental models that are used to mimic and evaluate the pathogenic mechanisms leading to these diseases of intestinal inflammation. We then highlight, as an example, how the use of different experimental models that focus on the role of Toll-like receptor 4 (TLR4) signaling in the gut has revealed important distinctions between the pathogenesis of IBD and necrotizing enterocolitis. Specifically, TLR4-mediated signaling plays a protective role in the development of Crohn’s disease and ulcerative colitis, whereas this signaling pathway plays a causative role in the development of necrotizing enterocolitis in the newborn small intestine by adversely affecting intestinal injury and repair mechanisms.
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spelling pubmed-31240492011-07-02 Worms, flies and four-legged friends: the applicability of biological models to the understanding of intestinal inflammatory diseases Lin, Joyce Hackam, David J. Dis Model Mech Commentary Diseases of intestinal inflammation, including Crohn’s disease, ulcerative colitis and necrotizing enterocolitis, cause substantial acute and chronic disability in a large proportion of the population. Crohn’s disease and ulcerative colitis, which are collectively referred to as inflammatory bowel disease (IBD), lead to recurrent episodes of intestinal dysfunction and systemic illness, whereas necrotizing enterocolitis is characterized by the development of dramatic and all too often fatal intestinal necrosis in infants. To determine the molecular underpinnings of these disorders, investigators have explored a variety of animal models that vary widely in their complexity. These experimental systems include the invertebrate nematode Caenorhabditis elegans, the more complex invertebrate Drosophila melanogaster, and vertebrate systems including mice, rats and other mammals. This review explores the experimental models that are used to mimic and evaluate the pathogenic mechanisms leading to these diseases of intestinal inflammation. We then highlight, as an example, how the use of different experimental models that focus on the role of Toll-like receptor 4 (TLR4) signaling in the gut has revealed important distinctions between the pathogenesis of IBD and necrotizing enterocolitis. Specifically, TLR4-mediated signaling plays a protective role in the development of Crohn’s disease and ulcerative colitis, whereas this signaling pathway plays a causative role in the development of necrotizing enterocolitis in the newborn small intestine by adversely affecting intestinal injury and repair mechanisms. The Company of Biologists Limited 2011-07 2011-06-13 /pmc/articles/PMC3124049/ /pubmed/21669933 http://dx.doi.org/10.1242/dmm.007252 Text en © 2011. Published by The Company of Biologists Ltd This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial Share Alike License (http://creativecommons.org/licenses/by-nc-sa/3.0), which permits unrestricted non-commercial use, distribution and reproduction in any medium provided that the original work is properly cited and all further distributions of the work or adaptation are subject to the same Creative Commons License terms.
spellingShingle Commentary
Lin, Joyce
Hackam, David J.
Worms, flies and four-legged friends: the applicability of biological models to the understanding of intestinal inflammatory diseases
title Worms, flies and four-legged friends: the applicability of biological models to the understanding of intestinal inflammatory diseases
title_full Worms, flies and four-legged friends: the applicability of biological models to the understanding of intestinal inflammatory diseases
title_fullStr Worms, flies and four-legged friends: the applicability of biological models to the understanding of intestinal inflammatory diseases
title_full_unstemmed Worms, flies and four-legged friends: the applicability of biological models to the understanding of intestinal inflammatory diseases
title_short Worms, flies and four-legged friends: the applicability of biological models to the understanding of intestinal inflammatory diseases
title_sort worms, flies and four-legged friends: the applicability of biological models to the understanding of intestinal inflammatory diseases
topic Commentary
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3124049/
https://www.ncbi.nlm.nih.gov/pubmed/21669933
http://dx.doi.org/10.1242/dmm.007252
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