@article{fdi:010037727,
  title = {{D}engue-virus-infected dendritic cells trigger vascular leakage through metalloproteinase overproduction},
  author = {{L}uplerdlop, {N}atthanej and {M}iss{\'e}, {D}oroth{\'e}e and {B}ray, {D}. and {D}eleuze, {V}. and {G}onzalez, {J}ean-{P}aul and {L}eardkamolkarn, {V}. and {Y}ssel, {H}. and {V}eas, {F}rancisco},
  editor = {},
  language = {{ENG}},
  abstract = {{D}engue virus ({DV}) is an important re-emerging arthropod-borne virus of global significance. {T}he defining characteristic of {DV} infection-associated pathology is haernorrhagic fever, which often leads to a fatal shock-like syndrome ({DHF}/{DSS}) owing to an increase in vascular endothelial permeability. {H}ere, 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 enclothelial permeability, but which are reduced by specific inhibitors and a neutralizing anti-{MMP}-9 antibody. {T}his permeability was associated with a loss of expression of the platelet enclothelial adhesion molecule 1 ({PECAM}-1) and vascular endothelium ({VE})-cadherin cell adhesion molecules and redistribution of {F}-actin fibres. {T}hese in vitro observations were confirmed in an in vivo vascular-leakage mouse model. {T}hese results provide a molecular basis for {DHF}/{DSS} that could be a basis for a general model of haernorrhagic fever-inducing viruses, and identify a new therapeutic approach for the treatment of viral-induced vascular leakage by specifically targeting gelatinolytic metal loproteases.},
  keywords = {endothelial cells ; haemorrhagic fever viruses ; matrix metalloprotease inhibitors ; plasma leakage ; {SB} 3{CT}},
  booktitle = {},
  journal = {{E}mbo {R}eports},
  volume = {7},
  numero = {11},
  pages = {1176--1181},
  ISSN = {1469-221{X}},
  year = {2006},
  DOI = {10.1038/sj.embor.7400814},
  URL = {https://www.documentation.ird.fr/hor/fdi:010037727},
}