| pubmed-article:19664145 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19664145 | lifeskim:mentions | umls-concept:C0004623 | lld:lifeskim |
| pubmed-article:19664145 | lifeskim:mentions | umls-concept:C0011777 | lld:lifeskim |
| pubmed-article:19664145 | lifeskim:mentions | umls-concept:C0332281 | lld:lifeskim |
| pubmed-article:19664145 | lifeskim:mentions | umls-concept:C0961814 | lld:lifeskim |
| pubmed-article:19664145 | lifeskim:mentions | umls-concept:C1533691 | lld:lifeskim |
| pubmed-article:19664145 | lifeskim:mentions | umls-concept:C1515655 | lld:lifeskim |
| pubmed-article:19664145 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:19664145 | pubmed:dateCreated | 2009-8-11 | lld:pubmed |
| pubmed-article:19664145 | pubmed:abstractText | Interleukin (IL)-22 production triggered by innate immune mechanisms has been identified as key to efficient intestinal anti-bacterial host defence and preservation of homeostasis. We hypothesized that glucocorticoid therapy may impair IL-22 expression, which should promote intestinal epithelial damage with the potential of subsequent bacterial translocation. High-dose corticosteroid therapy in Crohn's disease has been associated with an increased rate of abscess formation and ultimately with a higher risk of developing postoperative infectious complications, including abdominal sepsis. Thus, we sought to investigate effects of the prototypic glucocorticoid dexamethasone on IL-22 production in the context of bacterial infection. Enhanced IL-22 plasma levels were detectable in rat sepsis. Moreover, heat-inactivated Staphylococcus epidermidis, used as a prototypic activator of innate immunity, induced robust production of IL-22 by human peripheral blood mononuclear cells (PBMC). Here, we report for the first time that dexamethasone mediates remarkable suppression of IL-22 as detected in S. epidermidis-activated PBMC and rat sepsis, respectively. The data presented herein suggest that insufficient IL-22 function may contribute to impaired intestinal host defence in the context of corticosteroid therapy. | lld:pubmed |
| pubmed-article:19664145 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19664145 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19664145 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:19664145 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19664145 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19664145 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19664145 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19664145 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19664145 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19664145 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19664145 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19664145 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19664145 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:19664145 | pubmed:issn | 1365-2249 | lld:pubmed |
| pubmed-article:19664145 | pubmed:author | pubmed-author:BachmannMM | lld:pubmed |
| pubmed-article:19664145 | pubmed:author | pubmed-author:MühlHH | lld:pubmed |
| pubmed-article:19664145 | pubmed:author | pubmed-author:Pfeilschifter... | lld:pubmed |
| pubmed-article:19664145 | pubmed:author | pubmed-author:ZwisslerBB | lld:pubmed |
| pubmed-article:19664145 | pubmed:author | pubmed-author:HofstetterCC | lld:pubmed |
| pubmed-article:19664145 | pubmed:author | pubmed-author:SadikC DCD | lld:pubmed |
| pubmed-article:19664145 | pubmed:author | pubmed-author:ZieschéEE | lld:pubmed |
| pubmed-article:19664145 | pubmed:author | pubmed-author:ScheiermannPP | lld:pubmed |
| pubmed-article:19664145 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:19664145 | pubmed:volume | 157 | lld:pubmed |
| pubmed-article:19664145 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19664145 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19664145 | pubmed:pagination | 370-6 | lld:pubmed |
| pubmed-article:19664145 | pubmed:dateRevised | 2010-9-2 | lld:pubmed |
| pubmed-article:19664145 | pubmed:meshHeading | pubmed-meshheading:19664145... | lld:pubmed |
| pubmed-article:19664145 | pubmed:meshHeading | pubmed-meshheading:19664145... | lld:pubmed |
| pubmed-article:19664145 | pubmed:meshHeading | pubmed-meshheading:19664145... | lld:pubmed |
| pubmed-article:19664145 | pubmed:meshHeading | pubmed-meshheading:19664145... | lld:pubmed |
| pubmed-article:19664145 | pubmed:meshHeading | pubmed-meshheading:19664145... | lld:pubmed |
| pubmed-article:19664145 | pubmed:meshHeading | pubmed-meshheading:19664145... | lld:pubmed |
| pubmed-article:19664145 | pubmed:meshHeading | pubmed-meshheading:19664145... | lld:pubmed |
| pubmed-article:19664145 | pubmed:meshHeading | pubmed-meshheading:19664145... | lld:pubmed |
| pubmed-article:19664145 | pubmed:meshHeading | pubmed-meshheading:19664145... | lld:pubmed |
| pubmed-article:19664145 | pubmed:meshHeading | pubmed-meshheading:19664145... | lld:pubmed |
| pubmed-article:19664145 | pubmed:meshHeading | pubmed-meshheading:19664145... | lld:pubmed |
| pubmed-article:19664145 | pubmed:meshHeading | pubmed-meshheading:19664145... | lld:pubmed |
| pubmed-article:19664145 | pubmed:meshHeading | pubmed-meshheading:19664145... | lld:pubmed |
| pubmed-article:19664145 | pubmed:meshHeading | pubmed-meshheading:19664145... | lld:pubmed |
| pubmed-article:19664145 | pubmed:meshHeading | pubmed-meshheading:19664145... | lld:pubmed |
| pubmed-article:19664145 | pubmed:meshHeading | pubmed-meshheading:19664145... | lld:pubmed |
| pubmed-article:19664145 | pubmed:meshHeading | pubmed-meshheading:19664145... | lld:pubmed |
| pubmed-article:19664145 | pubmed:meshHeading | pubmed-meshheading:19664145... | lld:pubmed |
| pubmed-article:19664145 | pubmed:meshHeading | pubmed-meshheading:19664145... | lld:pubmed |
| pubmed-article:19664145 | pubmed:meshHeading | pubmed-meshheading:19664145... | lld:pubmed |
| pubmed-article:19664145 | pubmed:meshHeading | pubmed-meshheading:19664145... | lld:pubmed |
| pubmed-article:19664145 | pubmed:year | 2009 | lld:pubmed |
| pubmed-article:19664145 | pubmed:articleTitle | Dexamethasone suppresses interleukin-22 associated with bacterial infection in vitro and in vivo. | lld:pubmed |
| pubmed-article:19664145 | pubmed:affiliation | Pharmazentrum Frankfurt/ZAFES, Intensive Care Medicine and Pain Therapy, University Hospital Goethe University, 60590 Frankfurt am Main, Germany. | lld:pubmed |
| pubmed-article:19664145 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:19664145 | pubmed:publicationType | Comparative Study | lld:pubmed |
| pubmed-article:19664145 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| entrez-gene:500836 | entrezgene:pubmed | pubmed-article:19664145 | lld:entrezgene |
