Use of a human-like low-grade bacteremia model of experimental endocarditis to study the role of Staphylococcus aureus adhesins and platelet aggregation in early endocarditis.

Détails

ID Serval
serval:BIB_055F07556E9F
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Use of a human-like low-grade bacteremia model of experimental endocarditis to study the role of Staphylococcus aureus adhesins and platelet aggregation in early endocarditis.
Périodique
Infection and Immunity
Auteur(s)
Veloso T.R., Chaouch A., Roger T., Giddey M., Vouillamoz J., Majcherczyk P., Que Y.A., Rousson V., Moreillon P., Entenza J.M.
ISSN
1098-5522 (Electronic)
ISSN-L
0019-9567
Statut éditorial
Publié
Date de publication
2013
Peer-reviewed
Oui
Volume
81
Numéro
3
Pages
697-703
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Résumé
Animal models of infective endocarditis (IE) induced by high-grade bacteremia revealed the pathogenic roles of Staphylococcus aureus surface adhesins and platelet aggregation in the infection process. In humans, however, S. aureus IE possibly occurs through repeated bouts of low-grade bacteremia from a colonized site or intravenous device. Here we used a rat model of IE induced by continuous low-grade bacteremia to explore further the contributions of S. aureus virulence factors to the initiation of IE. Rats with aortic vegetations were inoculated by continuous intravenous infusion (0.0017 ml/min over 10 h) with 10(6) CFU of Lactococcus lactis pIL253 or a recombinant L. lactis strain expressing an individual S. aureus surface protein (ClfA, FnbpA, BCD, or SdrE) conferring a particular adhesive or platelet aggregation property. Vegetation infection was assessed 24 h later. Plasma was collected at 0, 2, and 6 h postinoculation to quantify the expression of tumor necrosis factor (TNF), interleukin 1α (IL-1α), IL-1β, IL-6, and IL-10. The percentage of vegetation infection relative to that with strain pIL253 (11%) increased when binding to fibrinogen was conferred on L. lactis (ClfA strain) (52%; P = 0.007) and increased further with adhesion to fibronectin (FnbpA strain) (75%; P < 0.001). Expression of fibronectin binding alone was not sufficient to induce IE (BCD strain) (10% of infection). Platelet aggregation increased the risk of vegetation infection (SdrE strain) (30%). Conferring adhesion to fibrinogen and fibronectin favored IL-1β and IL-6 production. Our results, with a model of IE induced by low-grade bacteremia, resembling human disease, extend the essential role of fibrinogen binding in the initiation of S. aureus IE. Triggering of platelet aggregation or an inflammatory response may contribute to or promote the development of IE.
Mots-clé
Adhesins, Bacterial/genetics, Adhesins, Bacterial/metabolism, Animals, Bacteremia/immunology, Bacterial Adhesion/physiology, Cytokines/genetics, Cytokines/metabolism, Endocarditis, Bacterial/immunology, Fibrinogen, Fibronectins, Gene Expression Regulation/immunology, Humans, Immobilized Proteins, Platelet Aggregation/immunology, Rats, Staphylococcus aureus/metabolism
Pubmed
Web of science
Open Access
Oui
Création de la notice
27/12/2012 15:07
Dernière modification de la notice
20/08/2019 13:27
Données d'usage