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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
5
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pubmed:dateCreated |
2003-8-20
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pubmed:abstractText |
Effects of adenoviral infection on in vivo responses to LPS mediated by TNF-alpha were evaluated in a murine model. Adenovirus-infected mice showed decreased mortality from fulminant hepatitis induced by administration of LPS or staphylococcal enterotoxin B in the presence of D-galactosamine. Importantly, TNF-alpha resistance genes within adenoviral E3 region were not required, because E1,E3-deleted vectors showed similar effects. Adenovirus-infected mice exhibited higher TNF-alpha levels after LPS stimulation, no difference in TNFR1 expression, and similar mortality from Fas-induced fulminant hepatitis. Decreased production of IL-6 and KC in response to exogenous TNF-alpha, in addition to protection from TNF-alpha, suggested that adenoviral infection results in TNF-alpha tolerance.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD95,
http://linkedlifedata.com/resource/pubmed/chemical/Autoantibodies,
http://linkedlifedata.com/resource/pubmed/chemical/Galactosamine,
http://linkedlifedata.com/resource/pubmed/chemical/Lipopolysaccharides,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Tumor Necrosis Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Tumor Necrosis Factor...,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0022-1767
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
171
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2453-60
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:12928393-Adenovirus Infections, Human,
pubmed-meshheading:12928393-Adenoviruses, Human,
pubmed-meshheading:12928393-Animals,
pubmed-meshheading:12928393-Antigens, CD,
pubmed-meshheading:12928393-Antigens, CD95,
pubmed-meshheading:12928393-Autoantibodies,
pubmed-meshheading:12928393-Cell Line,
pubmed-meshheading:12928393-Disease Models, Animal,
pubmed-meshheading:12928393-Female,
pubmed-meshheading:12928393-Galactosamine,
pubmed-meshheading:12928393-Humans,
pubmed-meshheading:12928393-Immune Tolerance,
pubmed-meshheading:12928393-Injections, Intraperitoneal,
pubmed-meshheading:12928393-Injections, Intravenous,
pubmed-meshheading:12928393-Lipopolysaccharides,
pubmed-meshheading:12928393-Liver,
pubmed-meshheading:12928393-Liver Failure,
pubmed-meshheading:12928393-Mice,
pubmed-meshheading:12928393-Mice, Inbred C57BL,
pubmed-meshheading:12928393-Mice, Inbred DBA,
pubmed-meshheading:12928393-Receptors, Tumor Necrosis Factor,
pubmed-meshheading:12928393-Receptors, Tumor Necrosis Factor, Type I,
pubmed-meshheading:12928393-Survival Analysis,
pubmed-meshheading:12928393-Tumor Necrosis Factor-alpha,
pubmed-meshheading:12928393-Up-Regulation
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pubmed:year |
2003
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pubmed:articleTitle |
Adenoviral infection decreases mortality from lipopolysaccharide-induced liver failure via induction of TNF-alpha tolerance.
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pubmed:affiliation |
Department of Internal Medicine, Division of Pulmonary, Critical Care, and Occupational Medicine, University of Iowa, 100 EMRB, Iowa City, IA 52242, USA. timur-yarovinsky@uiowa.edu
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.
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