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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3-5
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pubmed:dateCreated |
1993-8-19
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pubmed:abstractText |
Infection of murine PU5-1.8 macrophages and human monocytes by influenza A virus was associated with virus replication, release of tumor necrosis factor-alpha (TNF-alpha) and subsequent cell death. In the presence of small and by itself rather inefficient concentrations of lipopolysaccharide (LPS) or free lipid A (1 to 10 ng/ml), TNF-alpha production of virus-infected macrophages was strongly potentiated. LPS-triggered and enhanced TNF-alpha release from virus-infected macrophages was neither due to increased cell survival nor altered virus replication, potentiated TNF-alpha gene transcription, release of intracellularly stored TNF-alpha or shifts in the kinetics of TNF-alpha secretion. Influenza A virus infection alone induced a massive TNF-alpha mRNA accumulation which, however, was only weakly translated into bioactive TNF-alpha protein. When these virus-primed macrophages were exposed to LPS either simultaneously or up to 4 h after infection, an efficient and high translation into TNF-alpha protein occurred. Although the LPS-induced biochemical pathways leading to an augmented TNF-alpha production by virus-infected macrophages still remains unsolved, the findings suggest that the frequently observed serious clinical complications in the course of combined influenza A virus and bacterial infections may be due, at least in part, to an excessive release of cytokines such as TNF-alpha.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Dinoprostone,
http://linkedlifedata.com/resource/pubmed/chemical/Interferons,
http://linkedlifedata.com/resource/pubmed/chemical/Lipid A,
http://linkedlifedata.com/resource/pubmed/chemical/Lipopolysaccharides,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0171-2985
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
187
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
357-71
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:7687236-Animals,
pubmed-meshheading:7687236-Cell Death,
pubmed-meshheading:7687236-Cell Line,
pubmed-meshheading:7687236-Dinoprostone,
pubmed-meshheading:7687236-Electrophoresis, Polyacrylamide Gel,
pubmed-meshheading:7687236-Gene Expression,
pubmed-meshheading:7687236-Humans,
pubmed-meshheading:7687236-Immunoblotting,
pubmed-meshheading:7687236-Influenza A virus,
pubmed-meshheading:7687236-Interferons,
pubmed-meshheading:7687236-Lipid A,
pubmed-meshheading:7687236-Lipopolysaccharides,
pubmed-meshheading:7687236-Macrophages,
pubmed-meshheading:7687236-Monocytes,
pubmed-meshheading:7687236-RNA, Messenger,
pubmed-meshheading:7687236-Tumor Necrosis Factor-alpha,
pubmed-meshheading:7687236-Virus Replication
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pubmed:year |
1993
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pubmed:articleTitle |
The potentiating effect of LPS on tumor necrosis factor-alpha production by influenza A virus-infected macrophages.
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pubmed:affiliation |
Institute of Immunology, Philipps University, Marburg, Germany.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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