New concepts in the pathophysiology of infective endocarditis.
- Widmer E Department of Fundamental Microbiology, University of Lausanne, Biophore building, CH-1015 Lausanne, Switzerland.
- Que YA
- Entenza JM
- Moreillon P
- 2006-07-11
Published in:
- Current infectious disease reports. - 2006
English
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.
- Language
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- English
- Open access status
- green
- Identifiers
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- DOI 10.1007/s11908-006-0071-z
- PMID 16822370
- Persistent URL
- https://folia.unifr.ch/global/documents/55632
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