New concepts in the pathophysiology of infective endocarditis.

Détails

ID Serval
serval:BIB_DA4BA27157AE
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
New concepts in the pathophysiology of infective endocarditis.
Périodique
Current Infectious Disease Reports
Auteur(s)
Widmer E., Que Y.A., Entenza J.M., Moreillon P.
ISSN
1523-3847[print], 1523-3847[linking]
Statut éditorial
Publié
Date de publication
2006
Volume
8
Numéro
4
Pages
271-279
Langue
anglais
Résumé
Endocarditis pathogens colonize valves with pre-existing sterile vegetations or valves with minimal endothelial lesions. Inflamed endothelia produce cytokines, integrins, and tissue factor, which in turn attract fibronectin, monocytes, and platelets. Bacteria attaching to such structures further activate the cascade, becoming embedded and protected from host defenses. Staphylococcus aureus also actively invade the endothelium, causing apoptosis and endothelial damage. Knowledge of this interplay identifies host factors as potential therapeutic targets. Blocking infection by modulating host factors might be opportune because host factors are conserved. In contrast, interfering with bacterial virulence factors might be more complicated because they vary among different bacteria.
Pubmed
Création de la notice
07/04/2008 8:46
Dernière modification de la notice
03/03/2018 21:54
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