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Infect. Immun. doi:10.1128/IAI.01442-06
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Induction of Monocyte Chemotactic Protein-1 in colonic epithelial cells by Entamoeba histolytica is mediated via PI3 kinase/P65 pathway

Department of Microbiology and Infectious Diseases, University of Calgary, 3330 Hospital Drive NW, Calgary, Alberta, Canada T2N 4N1

^* To whom correspondence should be addressed. Email: kchadee{at}ucalgary.ca.

	Abstract

The role intestinal epithelial cells play in the pathogenesis of amebic colitis is poorly understood. Herein, we demonstrate that secreted and soluble Entamoeba histolytica proteins (SAP) induce the chemoattractant, Monocyte Chemotactic Protein (MCP)-expression in the colonic epithelial cell lines Caco-2, T84 and LS 174T. MCP-1 mRNA induction was both dose- and time-dependent with peak induction occurring at 8 h and with 100 µg/ml of SAP. Significant increase in MCP-1 protein expression was observed after 12 h. SAP failed to activate any of the MAP kinase pathways and IKK activity. Moreover, inhibiting the classical pathway of NF-B activation did not affect SAP induced MCP-1 expression. Instead, we find that it is dependent on posttranslational modification of NFB p65 subunit. SAP induced phosphorylation of p65 and enhanced NF-B transcriptional activity, which are PI3 kinase dependent. Treatment with PI3 kinase inhibitor LY290004 significantly abrogated the activation of Akt, p65 and MCP-1 mRNA induction. We conclude that colonic epithelial cells play a role in the initiation of inflammation by secreting chemokines in response to soluble ameba components.

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