Source:http://linkedlifedata.com/resource/pubmed/id/12370378
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
8
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| pubmed:dateCreated |
2002-10-8
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| pubmed:abstractText |
Hosts after severe burn injury are known to have a defect in the Th1 immune response and are susceptible to bacterial infections. We herein show that liver NK cells are potent IFN-gamma producers early after burn injury. However, when mice were injected with LPS 24 h after burn injury, IFN-gamma production from liver mononuclear cells (MNC; which we previously showed to be NK cells) was suppressed, and the serum IFN-gamma concentration did not increase, while serum IL-10 conversely increased compared with control mice. Interestingly, a single injection of IL-18 simultaneously with LPS greatly restored the serum IFN-gamma concentration in mice with burn injury and also increased IFN-gamma production from liver MNC. Nevertheless, a single IL-18 injection into mice simultaneously with LPS was no longer effective in the restoration of serum IFN-gamma and IFN-gamma production from the liver MNC at 7 days after burn injury, when mice were considered to be the most immunocompromised. However, IL-18 injections into mice on alternate days beginning 1 day after burn injury strongly up-regulated LPS-induced serum IFN-gamma levels and IFN-gamma production from liver and spleen MNC of mice 7 days after burn injury and down-regulated serum IL-10. Furthermore, similar IL-18 therapy up-regulated serum IFN-gamma levels in mice with experimental bacterial peritonitis 7 days after burn injury and greatly decreased mouse mortality. Thus, IL-18 therapy restores the Th1 response and may decrease the susceptibility to bacterial infection in mice with burn injury.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
AIM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:month |
Oct
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| pubmed:issn |
0022-1767
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:day |
15
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| pubmed:volume |
169
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
4437-42
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| pubmed:dateRevised |
2008-11-21
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| pubmed:meshHeading |
pubmed-meshheading:12370378-Animals,
pubmed-meshheading:12370378-Bacterial Infections,
pubmed-meshheading:12370378-Burns,
pubmed-meshheading:12370378-Cells, Cultured,
pubmed-meshheading:12370378-Down-Regulation,
pubmed-meshheading:12370378-Drug Administration Schedule,
pubmed-meshheading:12370378-Injections, Intraperitoneal,
pubmed-meshheading:12370378-Injections, Intravenous,
pubmed-meshheading:12370378-Interferon-gamma,
pubmed-meshheading:12370378-Interleukin-10,
pubmed-meshheading:12370378-Interleukin-18,
pubmed-meshheading:12370378-Killer Cells, Natural,
pubmed-meshheading:12370378-Lipopolysaccharides,
pubmed-meshheading:12370378-Liver,
pubmed-meshheading:12370378-Male,
pubmed-meshheading:12370378-Mice,
pubmed-meshheading:12370378-Mice, Inbred C57BL,
pubmed-meshheading:12370378-Peritonitis,
pubmed-meshheading:12370378-Spleen,
pubmed-meshheading:12370378-Treatment Failure,
pubmed-meshheading:12370378-Up-Regulation
|
| pubmed:year |
2002
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| pubmed:articleTitle |
IFN-gamma production from liver mononuclear cells of mice in burn injury as well as in postburn bacterial infection models and the therapeutic effect of IL-18.
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| pubmed:affiliation |
Division of Basic Traumatology, National Defense Medical College Research Institute, Namiki 3-2, Tokorozawa 359-8513, Japan.
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| pubmed:publicationType |
Journal Article
|