Source:http://linkedlifedata.com/resource/pubmed/id/17534407
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
2007-5-30
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pubmed:abstractText |
Human metapneumovirus and respiratory syncytial virus are RNA viruses associated with lower respiratory tract infections. Regular symptomatic re-infection and sequelae are common, particularly in individuals with pre-existing respiratory diseases, such as asthma. Our understanding of virus-dependent cytokine responses and potential differences between allergic asthmatics and non-asthmatics is limited. To test our hypothesis that adults with mild allergic asthma, the most common form of this disease, exhibit distinct pro-inflammatory responses, we developed a model using acute in vitro infection of fresh peripheral blood mononuclear cells. For both viruses, the production of innate-immunity-associated IL-6 and IL-10 was indistinguishable in the 2 populations. Type 1 cytokine production dominated adaptive immune responses in both asthmatic and non-asthmatic individuals. Surprisingly, asthmatics exhibited stronger pro-inflammatory IFNgamma production in response to human metapneumovirus than non-asthmatic adults (p = 0.01), with a similar, but statistically nonsignificant trend in the respiratory-syncytial-virus-stimulated response. Neutralizing IL-10 did not enhance the intensity of IFNgamma responses, demonstrating that this pro-inflammatory bias is not counter-regulated by IL-10. Finally, anti-TLR4 blocked lipopolysaccharide, but not respiratory-syncytial-virus-driven cytokine production. Collectively, the data demonstrate that asthma is characterized by markedly stronger pro-inflammatory IFNgamma responses to pneumoviruses than their non-asthmatic counterparts. This distinctive pattern of viral immunity may contribute to a worsening of asthma symptoms during respiratory virus infections.
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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/Antibodies, Monoclonal,
http://linkedlifedata.com/resource/pubmed/chemical/IL10 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/IL6 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-10,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-6,
http://linkedlifedata.com/resource/pubmed/chemical/Lipopolysaccharides,
http://linkedlifedata.com/resource/pubmed/chemical/TLR4 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Toll-Like Receptor 4
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0829-8211
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
85
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
252-8
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:17534407-Adolescent,
pubmed-meshheading:17534407-Adult,
pubmed-meshheading:17534407-Antibodies, Monoclonal,
pubmed-meshheading:17534407-Asthma,
pubmed-meshheading:17534407-Cell Line, Tumor,
pubmed-meshheading:17534407-Female,
pubmed-meshheading:17534407-Humans,
pubmed-meshheading:17534407-Immunity, Innate,
pubmed-meshheading:17534407-Interferon-gamma,
pubmed-meshheading:17534407-Interleukin-10,
pubmed-meshheading:17534407-Interleukin-6,
pubmed-meshheading:17534407-Lipopolysaccharides,
pubmed-meshheading:17534407-Male,
pubmed-meshheading:17534407-Metapneumovirus,
pubmed-meshheading:17534407-Middle Aged,
pubmed-meshheading:17534407-Respiratory Syncytial Virus Infections,
pubmed-meshheading:17534407-Respiratory Syncytial Viruses,
pubmed-meshheading:17534407-Toll-Like Receptor 4
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pubmed:year |
2007
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pubmed:articleTitle |
Adult asthmatics display exaggerated IFNgamma responses to human metapneumovirus and respiratory syncytial virus.
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pubmed:affiliation |
CIHR National Training Program in Allergy and Asthma Research, Department of Immunology, University of Manitoba, 603 Basic Medical Sciences Building, 730 William Ave, Winnipeg, MB R3E0W3, Canada.
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pubmed:publicationType |
Journal Article,
Clinical Trial,
Comparative Study,
Research Support, Non-U.S. Gov't
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