Direct interaction of iron-regulated surface determinant IsdB of Staphylococcus aureus with the GPIIb/IIIa receptor on platelets.
Microbiology (Reading)
; 156(Pt 3): 920-928, 2010 Mar.
Article
en En
| MEDLINE
| ID: mdl-20007649
ABSTRACT
The interaction of bacteria with platelets is implicated in the pathogenesis of endovascular infections, including infective endocarditis, of which Staphylococcus aureus is the leading cause. Several S. aureus surface proteins mediate aggregation of platelets by fibrinogen- or fibronectin-dependent processes, which also requires specific antibodies. In this study S. aureus was grown in iron-limited medium to mimic in vivo conditions in which iron is unavailable to pathogens. Under such conditions, a S. aureus mutant lacking the known platelet-activating surface proteins adhered directly to platelets in the absence of plasma proteins and triggered aggregation. Platelet adhesion and aggregation was prevented by inhibiting expression of iron-regulated surface determinant (Isd) proteins. Mutants defective in IsdB, but not IsdA or IsdH, were unable to adhere to or aggregate platelets. Antibodies to the platelet integrin GPIIb/IIIa inhibited platelet adhesion by IsdB-expressing strains, as did antagonists of GPIIb/IIIa. Surface plasmon resonance demonstrated that recombinant IsdB interacts directly with GPIIb/IIIa.
Texto completo:
1
Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Staphylococcus aureus
/
Proteínas Bacterianas
/
Plaquetas
/
Complejo GPIIb-IIIa de Glicoproteína Plaquetaria
/
Proteínas de Transporte de Catión
/
Hierro
Límite:
Humans
Idioma:
En
Revista:
Microbiology (Reading)
Asunto de la revista:
MICROBIOLOGIA
Año:
2010
Tipo del documento:
Article
País de afiliación:
Irlanda