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Giardia lamblia disrupts tight junctional ZO-1 and increases permeability in non-transformed human small intestinal epithelial monolayers: effects of epidermal growth factor

Published online by Cambridge University Press:  16 January 2003

A. G. BURET
Affiliation:
Department of Biological Sciences, Mucosal Inflammation Research Group, The University of Calgary, 2500 University Dr N.W., Calgary (Alberta), Canada T2N 1N4
K. MITCHELL
Affiliation:
Department of Biological Sciences, Mucosal Inflammation Research Group, The University of Calgary, 2500 University Dr N.W., Calgary (Alberta), Canada T2N 1N4
D. G. MUENCH
Affiliation:
Department of Biological Sciences, Mucosal Inflammation Research Group, The University of Calgary, 2500 University Dr N.W., Calgary (Alberta), Canada T2N 1N4
K. G. E. SCOTT
Affiliation:
Department of Biological Sciences, Mucosal Inflammation Research Group, The University of Calgary, 2500 University Dr N.W., Calgary (Alberta), Canada T2N 1N4
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Abstract

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In order to improve our understanding of the host cell–parasite interactions in giardiasis, this study assessed the effects of Giardia lamblia on epithelial permeability and tight junctional ZO-1, determined whether epidermal growth factor (EGF) may affect Giardia-induced epithelial injury, and evaluated if EGF modulates epithelial colonization by live G. lamblia trophozoites. Permeability was assessed in assays of trans-epithelial fluxes of FITC-dextran, and ZO-1 integrity was characterized by confocal laser immunofluorescence microscopy in confluent epithelial cell monolayers. G. lamblia significantly increased paracellular permeability and disrupted tight-junctional ZO-1 of a novel non-transformed human small intestinal epithelial cell line (SCBN). Pre-treatment with EGF prevented the development of these abnormalities and significantly inhibited attachment of live trophozoites to the enterocytes, independently of a direct microbiocidal action. These findings demonstrate that G. lamblia may cause intestinal pathophysiology by disrupting tight junctional ZO-1 and increasing epithelial permeability. Apical administration of EGF prevents these abnormalities, and reduces epithelial colonization by the live parasites.

Type
Research Article
Copyright
2002 Cambridge University Press