Role of sigmaB in the expression of Staphylococcus aureus cell wall adhesins ClfA and FnbA and contribution to infectivity in a rat model of experimental endocarditis.

Détails

ID Serval
serval:BIB_9B7E2760E376
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Role of sigmaB in the expression of Staphylococcus aureus cell wall adhesins ClfA and FnbA and contribution to infectivity in a rat model of experimental endocarditis.
Périodique
Infection and Immunity
Auteur(s)
Entenza J.M., Moreillon P., Senn M.M., Kormanec J., Dunman P.M., Berger-Bächi B., Projan S., Bischoff M.
ISSN
0019-9567[print], 0019-9567[linking]
Statut éditorial
Publié
Date de publication
2005
Volume
73
Numéro
2
Pages
990-998
Langue
anglais
Résumé
Isogenic Staphylococcus aureus strains with different capacities to produce sigma(B) activity were analyzed for their ability to attach to fibrinogen- or fibronectin-coated surfaces or platelet-fibrin clots and to cause endocarditis in rats. In comparison to the sigma(B)-deficient strain, BB255, which harbors an rsbU mutation, both rsbU-complemented and sigma(B)-overproducing derivatives exhibited at least five times greater attachment to fibrinogen- and fibronectin-coated surfaces and showed increased adherence to platelet-fibrin clots. No differences in adherence were seen between BB255 and a DeltarsbUVWsigB isogen. Northern blotting analyses revealed that transcription of clfA, encoding fibrinogen-binding protein clumping factor A, and fnbA, encoding fibronectin-binding protein A, were positively influenced by sigma(B). Sigma(B) overproduction resulted in a statistically significant increase in positive spleen cultures and enhanced bacterial densities in both the aortic vegetations and spleens at 16 h postinoculation. In contrast, at 72 h postinoculation, tissues infected with the sigma(B) overproducer had lower bacterial densities than did those infected with BB255. These results suggest that although sigma(B) appears to increase the adhesion of S. aureus to various host cell-matrix proteins in vitro, it has limited effect on pathogenesis in the rat endocarditis model. Sigma(B) appears to have a transient enhancing effect on bacterial density in the early stages of infection that is lost during progression.
Mots-clé
Adhesins, Bacterial/genetics, Adhesins, Bacterial/metabolism, Animals, Bacterial Proteins/metabolism, Cell Adhesion/physiology, Cell Wall, Endocarditis, Bacterial/metabolism, Endocarditis, Bacterial/microbiology, Fibrinogen/metabolism, Fibronectins/metabolism, Promoter Regions, Genetic, Rats, Sigma Factor/metabolism, Staphylococcus aureus/metabolism, Staphylococcus aureus/pathogenicity, alpha-Macroglobulins/metabolism
Pubmed
Web of science
Open Access
Oui
Création de la notice
24/01/2008 14:45
Dernière modification de la notice
20/08/2019 16:02
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