Source:http://linkedlifedata.com/resource/pubmed/id/19664145
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
2009-8-11
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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.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Dexamethasone,
http://linkedlifedata.com/resource/pubmed/chemical/Glucocorticoids,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-10,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-8,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukins,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/dexamethasone 21-phosphate,
http://linkedlifedata.com/resource/pubmed/chemical/interleukin-22
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
1365-2249
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
157
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
370-6
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pubmed:dateRevised |
2010-9-2
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pubmed:meshHeading |
pubmed-meshheading:19664145-Animals,
pubmed-meshheading:19664145-Case-Control Studies,
pubmed-meshheading:19664145-Cells, Cultured,
pubmed-meshheading:19664145-Depression, Chemical,
pubmed-meshheading:19664145-Dexamethasone,
pubmed-meshheading:19664145-Gene Expression,
pubmed-meshheading:19664145-Glucocorticoids,
pubmed-meshheading:19664145-Humans,
pubmed-meshheading:19664145-Interleukin-10,
pubmed-meshheading:19664145-Interleukin-8,
pubmed-meshheading:19664145-Interleukins,
pubmed-meshheading:19664145-Male,
pubmed-meshheading:19664145-Models, Animal,
pubmed-meshheading:19664145-Peritonitis,
pubmed-meshheading:19664145-RNA, Messenger,
pubmed-meshheading:19664145-Random Allocation,
pubmed-meshheading:19664145-Rats,
pubmed-meshheading:19664145-Rats, Sprague-Dawley,
pubmed-meshheading:19664145-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:19664145-Staphylococcal Infections,
pubmed-meshheading:19664145-Staphylococcus epidermidis
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pubmed:year |
2009
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pubmed:articleTitle |
Dexamethasone suppresses interleukin-22 associated with bacterial infection in vitro and in vivo.
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pubmed:affiliation |
Pharmazentrum Frankfurt/ZAFES, Intensive Care Medicine and Pain Therapy, University Hospital Goethe University, 60590 Frankfurt am Main, Germany.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
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