Source:http://linkedlifedata.com/resource/pubmed/id/19291698
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
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pubmed:dateCreated |
2009-4-13
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pubmed:abstractText |
iNOS plays an important role in mediating inflammation. In this study, we found that iNOS-derived NO was increased 2.4-fold in the serum samples of 101 patients infected with influenza A virus in comparison with samples of 105 healthy individuals. In A549 human lung epithelial cells, infection with influenza A virus or stimulation with poly(I:C)+IFN-gamma resulted in increased mRNA and protein levels of both IL-32 and iNOS, with subsequent release of NO. Over-expression of IL-32 resulted in upregulated iNOS expression with subsequent NO production. Knock down of IL-32 by IL-32-specific siRNA resulted in the inhibition of dsRNA-induced expression of iNOS and NO release, indicating that IL-32 is an upstream regulatory factor of dsRNA-triggered iNOS production. Surprisingly, over-expression of iNOS resulted in the reduction of IL-32 expression, and suppression of iNOS by the selective iNOS inhibitor S-methylisothiourea sulfate stimulated IL-32 expression, indicating that a negative feedback mechanism operates between the iNOS/NO and IL-32 systems. These findings suggest that influenza A virus infection activates IL-32 and iNOS expression by a heretofore unrecognized complex mechanism, in which the two pro-inflammatory factors regulate each other, involving positive and negative feedback regulatory loops.
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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/IL32 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukins,
http://linkedlifedata.com/resource/pubmed/chemical/NOS2 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase Type II,
http://linkedlifedata.com/resource/pubmed/chemical/Poly I-C,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Double-Stranded,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Small Interfering
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
1521-4141
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
39
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1019-24
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pubmed:dateRevised |
2011-10-27
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pubmed:meshHeading |
pubmed-meshheading:19291698-Adult,
pubmed-meshheading:19291698-Cell Line,
pubmed-meshheading:19291698-Cell Line, Tumor,
pubmed-meshheading:19291698-Enzyme Activation,
pubmed-meshheading:19291698-Feedback, Physiological,
pubmed-meshheading:19291698-Female,
pubmed-meshheading:19291698-Gene Knockdown Techniques,
pubmed-meshheading:19291698-Humans,
pubmed-meshheading:19291698-Influenza, Human,
pubmed-meshheading:19291698-Influenza A virus,
pubmed-meshheading:19291698-Interferon-gamma,
pubmed-meshheading:19291698-Interleukins,
pubmed-meshheading:19291698-Male,
pubmed-meshheading:19291698-Middle Aged,
pubmed-meshheading:19291698-Nitric Oxide,
pubmed-meshheading:19291698-Nitric Oxide Synthase Type II,
pubmed-meshheading:19291698-Poly I-C,
pubmed-meshheading:19291698-RNA, Double-Stranded,
pubmed-meshheading:19291698-RNA, Small Interfering
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pubmed:year |
2009
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pubmed:articleTitle |
Negative feedback regulation of IL-32 production by iNOS activation in response to dsRNA or influenza virus infection.
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pubmed:affiliation |
The State Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan, PR China.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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