New concepts in the pathophysiology of infective endocarditis.

Abstract:

: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.

journal_name

Curr Infect Dis Rep

authors

Widmer E,Que YA,Entenza JM,Moreillon P

doi

10.1007/s11908-006-0071-z

subject

Has Abstract

pub_date

2006-06-01 00:00:00

pages

271-9

issue

4

eissn

1523-3847

issn

1534-3146

journal_volume

8

pub_type

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