| pubmed-article:20566739 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20566739 | lifeskim:mentions | umls-concept:C0021853 | lld:lifeskim |
| pubmed-article:20566739 | lifeskim:mentions | umls-concept:C0108082 | lld:lifeskim |
| pubmed-article:20566739 | lifeskim:mentions | umls-concept:C0079904 | lld:lifeskim |
| pubmed-article:20566739 | lifeskim:mentions | umls-concept:C0441655 | lld:lifeskim |
| pubmed-article:20566739 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:20566739 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:20566739 | pubmed:dateCreated | 2010-8-3 | lld:pubmed |
| pubmed-article:20566739 | pubmed:abstractText | Vitamin D receptor (VDR) plays an essential role in gastrointestinal inflammation. Most investigations have focused on the immune response; however, how bacteria regulate VDR and how VDR modulates the nuclear factor (NF)-kappaB pathway in intestinal epithelial cells remain unexplored. This study investigated the effects of VDR ablation on NF-kappaB activation in intestinal epithelia and the role of enteric bacteria on VDR expression. We found that VDR(-/-) mice exhibited a pro-inflammatory bias. After Salmonella infection, VDR(-/-) mice had increased bacterial burden and mortality. Serum interleukin-6 in noninfected VDR(+/+) mice was undetectable, but was easily detectable in VDR(-/-) mice. NF-kappaB p65 formed a complex with VDR in noninfected wild-type mouse intestine. In contrast, deletion of VDR abolished VDR/P65 binding. P65 nuclear translocation occurred in colonic epithelial cells of untreated VDR(-/-) mice. VDR deletion also elevated NF-kappaB activity in intestinal epithelia. VDR was localized to the surface epithelia of germ-free mice, but to crypt epithelial cells in conventionalized mice. VDR expression, distribution, transcriptional activity, and target genes were regulated by Salmonella stimulation, independent of 1,25-dihydroxyvitamin D3. Our study demonstrates that commensal and pathogenic bacteria directly regulate colonic epithelial VDR expression and location in vivo. VDR negatively regulates bacterial-induced intestinal NF-kappaB activation and attenuates response to infection. Therefore, VDR is an important contributor to intestinal homeostasis and host protection from bacterial invasion and infection. | lld:pubmed |
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| pubmed-article:20566739 | pubmed:language | eng | lld:pubmed |
| pubmed-article:20566739 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20566739 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:20566739 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:20566739 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:20566739 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:20566739 | pubmed:issn | 1525-2191 | lld:pubmed |
| pubmed-article:20566739 | pubmed:author | pubmed-author:TagM HMH | lld:pubmed |
| pubmed-article:20566739 | pubmed:author | pubmed-author:LiJian-DongJD | lld:pubmed |
| pubmed-article:20566739 | pubmed:author | pubmed-author:SartorR... | lld:pubmed |
| pubmed-article:20566739 | pubmed:author | pubmed-author:LiYan ChunYC | lld:pubmed |
| pubmed-article:20566739 | pubmed:author | pubmed-author:WuShaopingS | lld:pubmed |
| pubmed-article:20566739 | pubmed:author | pubmed-author:LiaoAnne PAP | lld:pubmed |
| pubmed-article:20566739 | pubmed:author | pubmed-author:XiaYinglinY | lld:pubmed |
| pubmed-article:20566739 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:20566739 | pubmed:volume | 177 | lld:pubmed |
| pubmed-article:20566739 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:20566739 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:20566739 | pubmed:pagination | 686-97 | lld:pubmed |
| pubmed-article:20566739 | pubmed:dateRevised | 2011-8-3 | lld:pubmed |
