PMID: 15240718Jul 9, 2004Paper

Fluid shear regulates the kinetics and receptor specificity of Staphylococcus aureus binding to activated platelets

The Journal of Immunology : Official Journal of the American Association of Immunologists
Parag PawarK Konstantopoulos

Abstract

The interaction between surface components on the invading pathogen and host cells such as platelets plays a key role in the regulation of endovascular infections. However, the mechanisms mediating Staphylococcus aureus binding to platelets under shear remain largely unknown. This study was designed to investigate the kinetics and molecular requirements of platelet-S. aureus interactions in bulk suspensions subjected to a uniform shear field. Hydrodynamic shear-induced collisions augment platelet-S. aureus binding, which is further potentiated by platelet activation with stromal derived factor-1beta. Peak adhesion efficiency occurs at low shear (100 s(-1)) and decreases with increasing shear. The molecular interaction of platelet alpha(IIb)beta(3) with bacterial clumping factor A through fibrinogen bridging is necessary for stable bacterial binding to activated platelets under shear. Although this pathway is sufficient at low shear (</=400 s(-1)), the involvement of platelet gpIb and staphylococcal protein A through von Willebrand factor bridging is essential for optimal recruitment of S. aureus cells by platelets in the high shear regime. IgG plays an inhibitory role in the adhesion process, presumably by interfering with the ...Continue Reading

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Citations

Aug 9, 2006·European Journal of Clinical Investigation·S RindiP Speziale
Jan 6, 2007·Circulation Research·Philipp von Hundelshausen, Christian Weber
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