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Bacterial activation of -catenin signaling in human epithelia

¹Department of Pathology, University of Chicago, Chicago, Illinois 60637; and ²Epithelial Pathology Unit, Department of Pathology and Laboratory Medicine, Emory University, School of Medicine, Atlanta, Georgia 30322

Submitted 25 November 2003 ; accepted in final form 30 January 2004

The mucosal lining of the human intestine is constantly bathed in a milieu of commensal gut flora, the vast majority of these being nonpathogenic microorganisms. Here, we demonstrate that microbial-epithelial cell interactions not only affect proinflammatory pathways but also influence -catenin signaling, a key component in regulating epithelial cell proliferation. The nonpathogenic Salmonella strain PhoP^c activates the -catenin signaling pathway of human epithelia via a blockade of -catenin degradation. Normal -catenin ubiquitination necessary for constitutive -catenin degradation is abolished, allowing the accumulation and translocation of -catenin to the nucleus. Transcriptional activation mediated by the -catenin/T cell factor complex increases c-myc expression and enhances cell proliferation. We also show that the Salmonella effector protein AvrA is involved in modulating this -catenin activation. These data suggest that nonvirulent bacterial-epithelial interactions can influence -catenin signaling and cell growth control in a manner previously unsuspected.

host defense; inflammation; cellular proliferaton

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