Source:http://linkedlifedata.com/resource/pubmed/id/20505141
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2010-6-21
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pubmed:abstractText |
Respiratory viral infections have been implicated in exacerbations of allergic asthma, characterized by a Th2-biased immune response. Respiratory viruses target airway epithelial cells and dendritic cells (DCs). Their activation is, at least in part, mediated by the TLR3-dependent recognition of virus-derived dsRNA. To elucidate the role of epithelial cells and DCs and the implication of TLR3/Toll/IL-1R domain-containing adaptor-inducing IFN-beta (TRIF) pathway, we developed a mouse model of lung allergic exacerbation. The effect of intranasal administration of dsRNA in OVA-sensitized wild-type mice and TRIF(-/-) mice was evaluated on airway hyperresponsiveness and pulmonary inflammation. Our data demonstrated that treatment with dsRNA significantly increased the airway hyperresponsiveness, the lung inflammation, and the OVA-specific Th2 response. This was associated with an infiltrate of eosinophils, myeloid DCs, and T lymphocytes. TRIF activation was required for the development of dsRNA-induced exacerbation of the allergic reaction. Intratracheal transfer of IL-4/dsRNA/OVA-pretreated DCs also triggered exacerbation of the allergic reaction, whereas cells primed with dsRNA/OVA had a more limited effect. dsRNA-induced production of CCL20 by airway epithelium was associated with DC recruitment. In vivo and in vitro treatment with dsRNA amplified airway epithelial production of the pro-Th2 chemokines CCL11 and CCL17, their secretion being enhanced by Th2 cytokines. In conclusion, dsRNA derived from respiratory viruses trigger exacerbation of the pulmonary allergic reaction through TLR3/TRIF-dependent pathway. Moreover, Th2 cytokines participate in this process by modulating the response of airway epithelium and DCs to dsRNA.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adaptor Proteins, Vesicular...,
http://linkedlifedata.com/resource/pubmed/chemical/Allergens,
http://linkedlifedata.com/resource/pubmed/chemical/Ovalbumin,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Double-Stranded,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Viral,
http://linkedlifedata.com/resource/pubmed/chemical/TICAM-1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/TLR3 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Toll-Like Receptor 3
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
1550-6606
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:day |
1
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pubmed:volume |
185
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
451-9
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pubmed:meshHeading |
pubmed-meshheading:20505141-Adaptor Proteins, Vesicular Transport,
pubmed-meshheading:20505141-Allergens,
pubmed-meshheading:20505141-Animals,
pubmed-meshheading:20505141-Bronchial Hyperreactivity,
pubmed-meshheading:20505141-Dendritic Cells,
pubmed-meshheading:20505141-Disease Models, Animal,
pubmed-meshheading:20505141-Female,
pubmed-meshheading:20505141-Mice,
pubmed-meshheading:20505141-Mice, Inbred C57BL,
pubmed-meshheading:20505141-Mice, Knockout,
pubmed-meshheading:20505141-Ovalbumin,
pubmed-meshheading:20505141-RNA, Double-Stranded,
pubmed-meshheading:20505141-RNA, Viral,
pubmed-meshheading:20505141-Respiratory Hypersensitivity,
pubmed-meshheading:20505141-Respiratory Mucosa,
pubmed-meshheading:20505141-Signal Transduction,
pubmed-meshheading:20505141-Toll-Like Receptor 3
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pubmed:year |
2010
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pubmed:articleTitle |
Double-stranded RNA exacerbates pulmonary allergic reaction through TLR3: implication of airway epithelium and dendritic cells.
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pubmed:affiliation |
Infection Pulmonaire et Immunité Innée, Institut National de la Santé et de la Recherche Médicale, Unité 1019, France.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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