pubmed-article:15307168 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:15307168 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
pubmed-article:15307168 | lifeskim:mentions | umls-concept:C0021368 | lld:lifeskim |
pubmed-article:15307168 | lifeskim:mentions | umls-concept:C0021853 | lld:lifeskim |
pubmed-article:15307168 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
pubmed-article:15307168 | lifeskim:mentions | umls-concept:C0085246 | lld:lifeskim |
pubmed-article:15307168 | lifeskim:mentions | umls-concept:C0033684 | lld:lifeskim |
pubmed-article:15307168 | lifeskim:mentions | umls-concept:C0017337 | lld:lifeskim |
pubmed-article:15307168 | lifeskim:mentions | umls-concept:C0063700 | lld:lifeskim |
pubmed-article:15307168 | pubmed:issue | 9 | lld:pubmed |
pubmed-article:15307168 | pubmed:dateCreated | 2004-8-12 | lld:pubmed |
pubmed-article:15307168 | pubmed:abstractText | The transcription factor IFN regulatory factor-1 (IRF-1) regulates production and activity of many inflammatory mediators and cells. Here, we investigated the role of IRF-1 in intestinal inflammation using clinical and histologic scores; inflammatory mediators were also measured in colonic tissue. Dextran sulfate sodium (DSS) or trinitrobenzene sulfonic acid (TNBS) was administered to wild-type (WT) or IRF-1 knockout (KO) mice. DSS or TNBS led to a dramatic increase in lethality and colitis severity in IRF-1 KO compared with WT mice. Reduced levels of IFN-gamma and IL-18-binding protein (IL-18BP) were observed in the colon of IRF-1 KO mice, whereas levels of inducible nitric oxide synthase, cyclooxygenase-2, phosphorylated STAT-3, chemokines, TNF-alpha, IL-1beta, IL-15, and IL-18 were not significantly changed. Intestinal inflammation was not altered in IFN-gamma KO mice or in WT mice given neutralizing anti-IFN-gamma antibodies, but was increased in mice lacking TCR gamma delta lymphocytes, a population significantly decreased in the intestine of IRF-1-deficient mice. Administration of IL-18BP reversed the increased susceptibility of IRF-1 KO mice to DSS. These results suggest a protective role for IRF-1 in intestinal inflammation, with a possible anti-inflammatory and/or restorative role. IL-18BP and TCR gamma delta cells appear to be critical factors in the anti-inflammatory effects of IRF-1. | lld:pubmed |
pubmed-article:15307168 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15307168 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15307168 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15307168 | pubmed:language | eng | lld:pubmed |
pubmed-article:15307168 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15307168 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:15307168 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15307168 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15307168 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15307168 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15307168 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15307168 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15307168 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15307168 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15307168 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15307168 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:15307168 | pubmed:month | Sep | lld:pubmed |
pubmed-article:15307168 | pubmed:issn | 0014-2980 | lld:pubmed |
pubmed-article:15307168 | pubmed:author | pubmed-author:LehrHans AHA | lld:pubmed |
pubmed-article:15307168 | pubmed:author | pubmed-author:DinarelloChar... | lld:pubmed |
pubmed-article:15307168 | pubmed:author | pubmed-author:SiegmundBritt... | lld:pubmed |
pubmed-article:15307168 | pubmed:author | pubmed-author:FantuzziGiami... | lld:pubmed |
pubmed-article:15307168 | pubmed:author | pubmed-author:SenaldiGiorgi... | lld:pubmed |
pubmed-article:15307168 | pubmed:author | pubmed-author:SennelloJosep... | lld:pubmed |
pubmed-article:15307168 | pubmed:copyrightInfo | Copyright 2004 Wiley-VCH Verlag GmbH & Co. | lld:pubmed |
pubmed-article:15307168 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:15307168 | pubmed:volume | 34 | lld:pubmed |
pubmed-article:15307168 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:15307168 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:15307168 | pubmed:pagination | 2356-64 | lld:pubmed |
pubmed-article:15307168 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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pubmed-article:15307168 | pubmed:meshHeading | pubmed-meshheading:15307168... | lld:pubmed |
pubmed-article:15307168 | pubmed:year | 2004 | lld:pubmed |
pubmed-article:15307168 | pubmed:articleTitle | Frontline: interferon regulatory factor-1 as a protective gene in intestinal inflammation: role of TCR gamma delta T cells and interleukin-18-binding protein. | lld:pubmed |
pubmed-article:15307168 | pubmed:affiliation | Department of Medicine, University of Colorado Health Sciences Center, Denver, USA. | lld:pubmed |
pubmed-article:15307168 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:15307168 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:15307168 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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