Fibrinogen and fibronectin binding cooperate for valve infection and invasion in Staphylococcus aureus experimental endocarditis.

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State: Public
Version: author
Serval ID
serval:BIB_AC3F5C623CF4
Type
Article: article from journal or magazin.
Collection
Publications
Title
Fibrinogen and fibronectin binding cooperate for valve infection and invasion in Staphylococcus aureus experimental endocarditis.
Journal
Journal of Experimental Medicine
Author(s)
Que Y.A., Haefliger J.A., Piroth L., François P., Widmer E., Entenza J.M., Sinha B., Herrmann M., Francioli P., Vaudaux P., Moreillon P.
ISSN
0022-1007
Publication state
Published
Issued date
2005
Peer-reviewed
Oui
Volume
201
Number
10
Pages
1627-1635
Language
english
Notes
Publication types: Journal Article
Abstract
The expression of Staphylococcus aureus adhesins in Lactococcus lactis identified clumping factor A (ClfA) and fibronectin-binding protein A (FnBPA) as critical for valve colonization in rats with experimental endocarditis. This study further analyzed their role in disease evolution. Infected animals were followed for 3 d. ClfA-positive lactococci successfully colonized damaged valves, but were spontaneously eradicated over 48 h. In contrast, FnBPA-positive lactococci progressively increased bacterial titers in vegetations and spleens. At imaging, ClfA-positive lactococci were restricted to the vegetations, whereas FnBPA-positive lactococci also invaded the adjacent endothelium. This reflected the capacity of FnBPA to trigger cell internalization in vitro. Because FnBPA carries both fibrinogen- and fibronectin-binding domains, we tested the role of these functionalities by deleting the fibrinogen-binding domain of FnBPA and supplementing it with the fibrinogen-binding domain of ClfA in cis or in trans. Deletion of the fibrinogen-binding domain of FnBPA did not alter fibronectin binding and cell internalization in vitro. However, it totally abrogated valve infectivity in vivo. This ability was restored in cis by inserting the fibrinogen-binding domain of ClfA into truncated FnBPA, and in trans by coexpressing full-length ClfA and truncated FnBPA on two separate plasmids. Thus, fibrinogen and fibronectin binding could cooperate for S. aureus valve colonization and endothelial invasion in vivo.
Keywords
Adhesins, Bacterial, Animals, Bacterial Adhesion, Coagulase, Endocarditis, Bacterial, Endothelium, Vascular, Female, Fibrinogen, Fibronectins, Heart Valves, Lactococcus lactis, Protein Binding, Protein Structure, Tertiary, Rats, Rats, Wistar, Sequence Deletion, Spleen, Staphylococcal Infections, Staphylococcus aureus
Pubmed
Web of science
Open Access
Yes
Create date
07/04/2008 8:46
Last modification date
20/08/2019 16:16
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