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Crosstalk between NF-B and -catenin pathways in bacterial-colonized intestinal epithelial cells

¹Department of Pathology, ³The Inflammatory Bowel Disease Research Center, Department of Medicine, The University of Chicago, and ²Molecular Oncology Laboratory, Department of Surgery, The University of Chicago Medical Center, Chicago, Illinois

Submitted 16 November 2004 ; accepted in final form 8 March 2005

Salmonella-epithelial cell interactions are known to activate the proinflammatory NF-B signaling pathway and have recently been found to also influence the -catenin signaling pathway, an important regulator of epithelial cell proliferation and differentiation. Here, using polarized epithelial cell models, we demonstrate that these same bacteria-mediated effects also direct the molecular crosstalk between the NF-B and -catenin signaling pathways. Convergence of these two pathways is a result of the direct interaction between the NF-B p50 subunit and -catenin. We show that PhoP^c, the avirulent derivative of a wild-type Salmonella strain, attenuates NF-B activity by stabilizing the association of -catenin with NF-B. In cell lines expressing constitutively active -catenin, IB protein was indirectly stabilized and NF-B activity was repressed after wild-type Salmonella colonization. Accordingly, constitutively active -catenin was found to inhibit the secretion of IL-8. Thus our findings strongly suggest that the crosstalk between the -catenin and NF-B signaling pathways is an important regulator of intestinal inflammation.

bacteria; inflammation; nuclear factor-B; interleukin-8

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