Inflammatory bowel disease (IBD), the collective term for a group of chronic conditions characterised by inflammation of the gastrointestinal tract (including Crohn’s disease and ulcerative colitis), affects an estimated 1.4 million individuals in the US, and its incidence is increasing worldwide. Current treatments generally manage the symptoms rather than provide a cure, highlighting the need to develop effective molecular therapies. In this new study, Nathan Bahary and colleagues use zebrafish to demonstrate that a deficiency in phosphatidylinositol (PI) signalling could be involved in the pathogenesis of IBD. Abnormalities in PI signalling have been linked with gastrointestinal disorders; however, the mechanisms remained unclear. Here, the authors show that PI-synthesis-deficient zebrafish display persistent ER stress and disrupted intestinal architecture, resulting in IBD-like pathologies. These effects can be mimicked by pharmacological induction of ER stress, whereas abrogation of ER stress using chemical chaperones rescues the disease phenotype. These findings link PI signalling defects with ER-stress-mediated gastrointestinal disease, revealing a mechanism that could be targeted in the development of curative therapies for IBD. Page 93
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IN THIS ISSUE| 01 January 2014
Phosphatidylinositol signalling defects implicated in IBD
Online ISSN: 1754-8411
Print ISSN: 1754-8403
Written by editorial staff. © 2014. Published by The Company of Biologists Ltd.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.
Dis Model Mech (2014) 7 (1): 1.
Phosphatidylinositol signalling defects implicated in IBD. Dis Model Mech 1 January 2014; 7 (1): 1. doi:
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