| pubmed-article:10706609 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10706609 | lifeskim:mentions | umls-concept:C1456820 | lld:lifeskim |
| pubmed-article:10706609 | lifeskim:mentions | umls-concept:C0013081 | lld:lifeskim |
| pubmed-article:10706609 | lifeskim:mentions | umls-concept:C1512032 | lld:lifeskim |
| pubmed-article:10706609 | lifeskim:mentions | umls-concept:C0033268 | lld:lifeskim |
| pubmed-article:10706609 | lifeskim:mentions | umls-concept:C1328650 | lld:lifeskim |
| pubmed-article:10706609 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:10706609 | pubmed:dateCreated | 2000-4-25 | lld:pubmed |
| pubmed-article:10706609 | pubmed:abstractText | We recently showed that adenoviral transfer and expression of the Lps(d)/Ran gene isolated from endotoxin-resistant C3H/HeJ mice could protect endotoxin-sensitive mice from endotoxic shock. Elevation of proinflammatory cytokines, such as tumor necrosis factor alpha (TNF-alpha), is thought to be essential for the development of septic shock. To investigate the extent to which Lps(d)/Ran affects TNF-alpha production, we transduced primary macrophages from endotoxin-sensitive and -resistant mice with adenoviral vectors expressing the wild-type and the mutant Lps/Ran cDNAs and other control genes, and compared the amount of TNF-alpha produced by these various transduced macrophages. Successful transfer and expression of Lps(d)/Ran cDNA in endotoxin-sensitive C3H/HeOuJ macrophages reduced TNF-alpha production upon lipopolysaccharide (LPS) stimulation, as compared with macrophages transduced with vectors expressing the wild-type Lps(n)/Ran cDNA, the green fluorescent protein gene, or the lacZ gene. On the other hand, successful transfer and expression of the wild-type Lps(n)/Ran cDNA in primary macrophages from endotoxin-resistant C3H/HeJ mice failed to induce TNF-alpha production to any significant extent unless a very high LPS concentration was used. Given our previous demonstration that Lps(n)/Ran functions effectively in restoring LPS responsiveness in B cells from C3H/HeJ mice, we conclude that Lps/Ran is involved in a CD14-independent signal transduction pathway. This dominant negative down-regulation by Lps(d)/Ran on TNF-alpha production by macrophages and probably other innate immune responses may be key to the development of an effective gene therapy for endotoxic or septic shock. | lld:pubmed |
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| pubmed-article:10706609 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10706609 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10706609 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:10706609 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:10706609 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10706609 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:10706609 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:10706609 | pubmed:author | pubmed-author:SultzerB MBM | lld:pubmed |
| pubmed-article:10706609 | pubmed:author | pubmed-author:KanY WYW | lld:pubmed |
| pubmed-article:10706609 | pubmed:author | pubmed-author:FanPP | lld:pubmed |
| pubmed-article:10706609 | pubmed:author | pubmed-author:ZhaoFF | lld:pubmed |
| pubmed-article:10706609 | pubmed:author | pubmed-author:YuanQQ | lld:pubmed |
| pubmed-article:10706609 | pubmed:author | pubmed-author:ChengC WCW | lld:pubmed |
| pubmed-article:10706609 | pubmed:author | pubmed-author:WongP MPM | lld:pubmed |
| pubmed-article:10706609 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10706609 | pubmed:day | 14 | lld:pubmed |
| pubmed-article:10706609 | pubmed:volume | 97 | lld:pubmed |
| pubmed-article:10706609 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10706609 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10706609 | pubmed:pagination | 2852-7 | lld:pubmed |
| pubmed-article:10706609 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:10706609 | pubmed:year | 2000 | lld:pubmed |
| pubmed-article:10706609 | pubmed:articleTitle | Dominant negative down-regulation of endotoxin-induced tumor necrosis factor alpha production by Lps(d)/Ran. | lld:pubmed |
| pubmed-article:10706609 | pubmed:affiliation | Department of Pathology and Laboratory Medicine, Fels Institute, Temple University School of Medicine, Philadelphia, PA 19140, USA. | lld:pubmed |
| pubmed-article:10706609 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10706609 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:10706609 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
