| pubmed-article:12370378 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12370378 | lifeskim:mentions | umls-concept:C0004623 | lld:lifeskim |
| pubmed-article:12370378 | lifeskim:mentions | umls-concept:C0006434 | lld:lifeskim |
| pubmed-article:12370378 | lifeskim:mentions | umls-concept:C0026339 | lld:lifeskim |
| pubmed-article:12370378 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:12370378 | lifeskim:mentions | umls-concept:C0026336 | lld:lifeskim |
| pubmed-article:12370378 | lifeskim:mentions | umls-concept:C0383327 | lld:lifeskim |
| pubmed-article:12370378 | lifeskim:mentions | umls-concept:C0023884 | lld:lifeskim |
| pubmed-article:12370378 | lifeskim:mentions | umls-concept:C0806987 | lld:lifeskim |
| pubmed-article:12370378 | lifeskim:mentions | umls-concept:C1527144 | lld:lifeskim |
| pubmed-article:12370378 | lifeskim:mentions | umls-concept:C0033268 | lld:lifeskim |
| pubmed-article:12370378 | pubmed:issue | 8 | lld:pubmed |
| pubmed-article:12370378 | pubmed:dateCreated | 2002-10-8 | lld:pubmed |
| pubmed-article:12370378 | 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. | lld:pubmed |
| pubmed-article:12370378 | pubmed:language | eng | lld:pubmed |
| pubmed-article:12370378 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12370378 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:12370378 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12370378 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12370378 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12370378 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12370378 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12370378 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:12370378 | pubmed:issn | 0022-1767 | lld:pubmed |
| pubmed-article:12370378 | pubmed:author | pubmed-author:IwaiTakehisaT | lld:pubmed |
| pubmed-article:12370378 | pubmed:author | pubmed-author:ShinomiyaNari... | lld:pubmed |
| pubmed-article:12370378 | pubmed:author | pubmed-author:SekiShuhjiS | lld:pubmed |
| pubmed-article:12370378 | pubmed:author | pubmed-author:HabuYoshikoY | lld:pubmed |
| pubmed-article:12370378 | pubmed:author | pubmed-author:HiraideHoshio... | lld:pubmed |
| pubmed-article:12370378 | pubmed:author | pubmed-author:YamauchiAkira... | lld:pubmed |
| pubmed-article:12370378 | pubmed:author | pubmed-author:KinoshitaMana... | lld:pubmed |
| pubmed-article:12370378 | pubmed:author | pubmed-author:AmiKatsunoriK | lld:pubmed |
| pubmed-article:12370378 | pubmed:author | pubmed-author:NishikageTets... | lld:pubmed |
| pubmed-article:12370378 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12370378 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:12370378 | pubmed:volume | 169 | lld:pubmed |
| pubmed-article:12370378 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12370378 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12370378 | pubmed:pagination | 4437-42 | lld:pubmed |
| pubmed-article:12370378 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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| pubmed-article:12370378 | pubmed:year | 2002 | lld:pubmed |
| pubmed-article:12370378 | 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. | lld:pubmed |
| pubmed-article:12370378 | pubmed:affiliation | Division of Basic Traumatology, National Defense Medical College Research Institute, Namiki 3-2, Tokorozawa 359-8513, Japan. | lld:pubmed |
| pubmed-article:12370378 | pubmed:publicationType | Journal Article | lld:pubmed |
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