pubmed-article:7594556 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:7594556 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
pubmed-article:7594556 | lifeskim:mentions | umls-concept:C0011065 | lld:lifeskim |
pubmed-article:7594556 | lifeskim:mentions | umls-concept:C0085295 | lld:lifeskim |
pubmed-article:7594556 | lifeskim:mentions | umls-concept:C0031154 | lld:lifeskim |
pubmed-article:7594556 | lifeskim:mentions | umls-concept:C0205227 | lld:lifeskim |
pubmed-article:7594556 | pubmed:issue | 11 | lld:pubmed |
pubmed-article:7594556 | pubmed:dateCreated | 1995-12-28 | lld:pubmed |
pubmed-article:7594556 | pubmed:abstractText | IL-10 production during endotoxic shock is part of a protective mechanism that involves IL-10-induced inhibition of TNF synthesis. We sought to determine the role of IL-10 in septic peritonitis induced by cecal ligation and puncture (CLP). CLP led to a rapid induction of IL-10 mRNA in various organs of C57BI/6 mice. In liver, IL-10 mRNA was detectable within 1 h following CLP, while in spleen and lungs, IL-10 mRNA was detected from 2 to 4 h and onward. IL-10 protein became detectable in plasma 2 h after CLP, reaching peak concentrations after 12 h (12.7 +/- 5.7 ng/ml). Pretreatment (-2 h) with anti-IL-10 mAb resulted in higher plasma TNF levels following CLP when compared with mice treated with control mAb. Plasma IL-1 activity and IFN-gamma remained undetectable in virtually all mice. Anti-IL-10 enhanced mortality after CLP (p < 0.05 by log-rank test). Addition of anti-TNF mAb did not influence the increased mortality associated with anti-IL-10 treatment. Septic peritonitis is associated with sustained production of IL-10 in various organs, which serves to protect the host against lethality. | lld:pubmed |
pubmed-article:7594556 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:7594556 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:7594556 | pubmed:language | eng | lld:pubmed |
pubmed-article:7594556 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:7594556 | pubmed:citationSubset | AIM | lld:pubmed |
pubmed-article:7594556 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:7594556 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:7594556 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:7594556 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:7594556 | pubmed:month | Dec | lld:pubmed |
pubmed-article:7594556 | pubmed:issn | 0022-1767 | lld:pubmed |
pubmed-article:7594556 | pubmed:author | pubmed-author:LowryS FSF | lld:pubmed |
pubmed-article:7594556 | pubmed:author | pubmed-author:GoldmanMM | lld:pubmed |
pubmed-article:7594556 | pubmed:author | pubmed-author:BermanLL | lld:pubmed |
pubmed-article:7594556 | pubmed:author | pubmed-author:MoldawerL LLL | lld:pubmed |
pubmed-article:7594556 | pubmed:author | pubmed-author:BuurmanW AWA | lld:pubmed |
pubmed-article:7594556 | pubmed:author | pubmed-author:KeoghC VCV | lld:pubmed |
pubmed-article:7594556 | pubmed:author | pubmed-author:MarchantAA | lld:pubmed |
pubmed-article:7594556 | pubmed:author | pubmed-author:NguyenLL | lld:pubmed |
pubmed-article:7594556 | pubmed:author | pubmed-author:LazarusD DDD | lld:pubmed |
pubmed-article:7594556 | pubmed:author | pubmed-author:van der... | lld:pubmed |
pubmed-article:7594556 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:7594556 | pubmed:day | 1 | lld:pubmed |
pubmed-article:7594556 | pubmed:volume | 155 | lld:pubmed |
pubmed-article:7594556 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:7594556 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:7594556 | pubmed:pagination | 5397-401 | lld:pubmed |
pubmed-article:7594556 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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pubmed-article:7594556 | pubmed:meshHeading | pubmed-meshheading:7594556-... | lld:pubmed |
pubmed-article:7594556 | pubmed:year | 1995 | lld:pubmed |
pubmed-article:7594556 | pubmed:articleTitle | Endogenous IL-10 protects mice from death during septic peritonitis. | lld:pubmed |
pubmed-article:7594556 | pubmed:affiliation | Cornell University Medical College, Department of Surgery, New York, NY 10021, USA. | lld:pubmed |
pubmed-article:7594556 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:7594556 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:7594556 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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