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Type: Journal article
Title: Rapid disruption of intestinal barrier function by gliadin involves altered expression of apical junctional proteins
Author: Sander, G.
Cummins, A.
Powell, B.
Citation: FEBS Letters, 2005; 579(21):4851-4855
Publisher: Elsevier Science BV
Issue Date: 2005
ISSN: 0014-5793
Statement of
Guy R. Sander, Adrian G. Cummins, d and Barry C. Powell
Abstract: Coeliac disease is a chronic enteropathy caused by the ingestion of wheat gliadin and other cereal prolamines derived from rye and barley. In the present work, we investigated the mechanisms underlying altered barrier function properties exerted by gliadin-derived peptides in human Caco-2 intestinal epithelial cells. We demonstrate that gliadin alters barrier function almost immediately by decreasing transepithelial resistance and increasing permeability to small molecules (4 kDa). Gliadin caused a reorganisation of actin filaments and altered expression of the tight junction proteins occludin, claudin-3 and claudin-4, the TJ-associated protein ZO-1 and the adherens junction protein E-cadherin.
Keywords: Coeliac
Barrier function
Tight junction
Adherens junction
Description: Copyright © 2005 Federation of European Biochemical Societies Published by Elsevier B.V.
DOI: 10.1016/j.febslet.2005.07.066
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Appears in Collections:Aurora harvest 6
Paediatrics publications

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