| pubmed-article:12717626 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12717626 | lifeskim:mentions | umls-concept:C0014833 | lld:lifeskim |
| pubmed-article:12717626 | lifeskim:mentions | umls-concept:C0254610 | lld:lifeskim |
| pubmed-article:12717626 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
| pubmed-article:12717626 | lifeskim:mentions | umls-concept:C1514559 | lld:lifeskim |
| pubmed-article:12717626 | lifeskim:mentions | umls-concept:C0036974 | lld:lifeskim |
| pubmed-article:12717626 | lifeskim:mentions | umls-concept:C0021467 | lld:lifeskim |
| pubmed-article:12717626 | lifeskim:mentions | umls-concept:C0333516 | lld:lifeskim |
| pubmed-article:12717626 | lifeskim:mentions | umls-concept:C0021469 | lld:lifeskim |
| pubmed-article:12717626 | pubmed:issue | 9 | lld:pubmed |
| pubmed-article:12717626 | pubmed:dateCreated | 2003-4-28 | lld:pubmed |
| pubmed-article:12717626 | pubmed:abstractText | Interleukin (IL)-15, a potent inhibitor of tumor necrosis factor (TNF)-alpha-mediated apoptosis, causes multiple organ failure during endotoxic shock. We investigated the potential role of IL-15 in protection against Escherichia coli-induced shock by using IL-15 transgenic (Tg) mice. These mice were resistant to an otherwise lethal challenge with E. coli, although bacterial burden and serum levels of TNF-alpha were similar in non-Tg mice. Apoptosis in cells of the peritoneal cavity, liver, spleen, or lung was significantly suppressed in IL-15 Tg mice after E. coli infection. Peritoneal cells from naive IL-15 Tg mice were also resistant to TNF-alpha-induced apoptosis in vitro, and neutralization of endogenous IL-15 significantly aggravated TNF-alpha-induced apoptosis. Exogenous IL-15 prevented TNF-alpha-induced apoptosis in normal mice in vitro and improved the survival rate after E. coli challenge. These results suggest that IL-15 overexpression can prevent TNF-alpha-induced apoptosis and protect against E. coli-induced shock, indicating a possible therapeutic application of IL-15 for septic shock. | lld:pubmed |
| pubmed-article:12717626 | pubmed:language | eng | lld:pubmed |
| pubmed-article:12717626 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12717626 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:12717626 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12717626 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12717626 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12717626 | pubmed:month | May | lld:pubmed |
| pubmed-article:12717626 | pubmed:issn | 0022-1899 | lld:pubmed |
| pubmed-article:12717626 | pubmed:author | pubmed-author:NishimuraHito... | lld:pubmed |
| pubmed-article:12717626 | pubmed:author | pubmed-author:YoshikaiYasun... | lld:pubmed |
| pubmed-article:12717626 | pubmed:author | pubmed-author:YajimaToshiki... | lld:pubmed |
| pubmed-article:12717626 | pubmed:author | pubmed-author:NimuraYujiY | lld:pubmed |
| pubmed-article:12717626 | pubmed:author | pubmed-author:MatsuguchiTet... | lld:pubmed |
| pubmed-article:12717626 | pubmed:author | pubmed-author:HiromatsuTaka... | lld:pubmed |
| pubmed-article:12717626 | pubmed:author | pubmed-author:WajjwalkuWora... | lld:pubmed |
| pubmed-article:12717626 | pubmed:author | pubmed-author:AraiToshiyuki... | lld:pubmed |
| pubmed-article:12717626 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12717626 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:12717626 | pubmed:volume | 187 | lld:pubmed |
| pubmed-article:12717626 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12717626 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12717626 | pubmed:pagination | 1442-51 | lld:pubmed |
| pubmed-article:12717626 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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| pubmed-article:12717626 | pubmed:meshHeading | pubmed-meshheading:12717626... | lld:pubmed |
| pubmed-article:12717626 | pubmed:year | 2003 | lld:pubmed |
| pubmed-article:12717626 | pubmed:articleTitle | Overexpression of interleukin-15 protects against Escherichia coli-induced shock accompanied by inhibition of tumor necrosis factor-alpha-induced apoptosis. | lld:pubmed |
| pubmed-article:12717626 | pubmed:affiliation | Laboratory of Host Defense and Germfree Life, Research Institute for Disease Mechanism and Control, Nagoya University School of Medicine, Nagoya, Japan. takasi-h@med.nagoya-u.ac.jp | lld:pubmed |
| pubmed-article:12717626 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:12717626 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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