serval:BIB_DA4BA27157AE
New concepts in the pathophysiology of infective endocarditis.
10.1007/s11908-006-0071-z
16822370
Widmer
E.
author
Que
Y.A.
author
Entenza
J.M.
author
Moreillon
P.
author
article
2006
Current Infectious Disease Reports
1523-3847[print], 1523-3847[linking]
journal
8
4
271-279
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.
eng
60_published
true
University of Lausanne
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