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pubmed-article:15790758pubmed:abstractTextSalmonella-epithelial cell interactions are known to activate the proinflammatory NF-kappaB signaling pathway and have recently been found to also influence the beta-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-kappaB and beta-catenin signaling pathways. Convergence of these two pathways is a result of the direct interaction between the NF-kappaB p50 subunit and beta-catenin. We show that PhoP(c), the avirulent derivative of a wild-type Salmonella strain, attenuates NF-kappaB activity by stabilizing the association of beta-catenin with NF-kappaB. In cell lines expressing constitutively active beta-catenin, IkappaBalpha protein was indirectly stabilized and NF-kappaB activity was repressed after wild-type Salmonella colonization. Accordingly, constitutively active beta-catenin was found to inhibit the secretion of IL-8. Thus our findings strongly suggest that the crosstalk between the beta-catenin and NF-kappaB signaling pathways is an important regulator of intestinal inflammation.lld:pubmed
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pubmed-article:15790758pubmed:articleTitleCrosstalk between NF-kappaB and beta-catenin pathways in bacterial-colonized intestinal epithelial cells.lld:pubmed
pubmed-article:15790758pubmed:affiliationDepartment of Pathology, University of Chicago, 5841 S. Maryland Ave., Chicago, IL 60637, USA. jsun@bsd.uchicago.edulld:pubmed
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