rdf:type |
|
lifeskim:mentions |
|
pubmed:issue |
11
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pubmed:dateCreated |
2006-11-1
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pubmed:abstractText |
Dengue virus (DV) is an important re-emerging arthropod-borne virus of global significance. The defining characteristic of DV infection-associated pathology is haemorrhagic fever, which often leads to a fatal shock-like syndrome (DHF/DSS) owing to an increase in vascular endothelial permeability. Here, we show, in a viral dose-dependent manner, that DV-infected immature dendritic cells overproduce soluble gelatinolytic matrix metalloproteinase (MMP)-9-and to a lesser extent MMP-2-which enhances endothelial permeability, but which are reduced by specific inhibitors and a neutralizing anti-MMP-9 antibody. This permeability was associated with a loss of expression of the platelet endothelial adhesion molecule 1 (PECAM-1) and vascular endothelium (VE)-cadherin cell adhesion molecules and redistribution of F-actin fibres. These in vitro observations were confirmed in an in vivo vascular-leakage mouse model. These results provide a molecular basis for DHF/DSS that could be a basis for a general model of haemorrhagic fever-inducing viruses, and identify a new therapeutic approach for the treatment of viral-induced vascular leakage by specifically targeting gelatinolytic metalloproteases.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/17028575,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17028575-10341210,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17028575-10469270,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/17028575-16316467,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/17028575-6607288,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17028575-9327744,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17028575-9346290,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17028575-9626949,
http://linkedlifedata.com/resource/pubmed/commentcorrection/17028575-9665979
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pubmed:language |
eng
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pubmed:journal |
|
pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
1469-221X
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pubmed:author |
|
pubmed:issnType |
Print
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pubmed:volume |
7
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1176-81
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:17028575-Capillary Permeability,
pubmed-meshheading:17028575-Cells, Cultured,
pubmed-meshheading:17028575-Culture Media, Conditioned,
pubmed-meshheading:17028575-Dendritic Cells,
pubmed-meshheading:17028575-Dengue Hemorrhagic Fever,
pubmed-meshheading:17028575-Dengue Virus,
pubmed-meshheading:17028575-Endothelium, Vascular,
pubmed-meshheading:17028575-Humans,
pubmed-meshheading:17028575-Metalloproteases,
pubmed-meshheading:17028575-Syndrome
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pubmed:year |
2006
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pubmed:articleTitle |
Dengue-virus-infected dendritic cells trigger vascular leakage through metalloproteinase overproduction.
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pubmed:affiliation |
Institut de Recherche pour le Développement, IRD, Immunologie Virale et Moléculaire, UR178 IFR122, 34094 Montpellier, France.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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