Fulltext

New concepts in the pathophysiology of infective endocarditis

Widmer, Eleonora ; Que, Yok-Ai ; Entenza, José ; Moreillon, Philippe

In: Current Infectious Disease Reports, 2006, vol. 8, no. 4, p. 271-279

Ajouter à la liste personnelle
    Titre
    • New concepts in the pathophysiology of infective endocarditis
    Auteur
    • Widmer, Eleonora
    • Que, Yok-Ai
    • Entenza, José
    • Moreillon, Philippe. Department of Fundamental Microbiology, University of Lausanne, Biophore building, CH-1015, Lausanne, Switzerland
    Type de document
    • Postprint
    Langue
    • Anglais
    Publié dans
    • Current Infectious Disease Reports, 2006, vol. 8, no. 4, p. 271-279. Current Medicine Group
    Autre version électronique
    Classification
    • Santé
    Identifiant OAI-PMH
    • oai:doc.rero.ch:317328
    Summary
    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