Literature DB >> 16857949

Staphylococcus aureus adhesion via Spa, ClfA, and SdrCDE to immobilized platelets demonstrates shear-dependent behavior.

Niraj Procopio Evagrio George1, Qi Wei, Pyong Kyun Shin, Konstantinos Konstantopoulos, Julia M Ross.   

Abstract

OBJECTIVE: The objective of this study is to delineate the molecular mechanisms responsible for Staphylococcus aureus-platelet adhesion as a function of physiologically relevant wall shear stresses. METHODS AND
RESULTS: A parallel plate flow chamber was used to quantify adhesion of wild-type, Spa-, ClfA- and SdrCDE- strains to immobilized platelet layers. In the absence of plasma, adhesion increases with increasing wall shear rate from 100 to 5000 seconds(-1). The presence of plasma significantly enhances adhesion at all shear levels. Addition of exogenous fibrinogen yields adhesion levels similar to plasma in the lower shear regimes, but has a diminishing effect on potentiating adhesion at higher shear rates. Alternatively, as shear rate increases von Willebrand factor (VWF) plays an increasingly significant role in mediating binding.
CONCLUSIONS: Addition of plasma proteins potentiates S aureus-platelet interactions at all shear rates examined. Whereas fibrinogen plays a significant role in all shear regimes, VWF mediation becomes increasingly important as wall shear rate increases. Fibrinogen binding is dependent on bacterial adhesins ClfA and SdrCDE whereas Spa is the dominant receptor for VWF.

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Year:  2006        PMID: 16857949     DOI: 10.1161/01.ATV.0000237606.90253.94

Source DB:  PubMed          Journal:  Arterioscler Thromb Vasc Biol        ISSN: 1079-5642            Impact factor:   8.311


  19 in total

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10.  Proteomic analysis of Staphylococcus aureus biofilm cells grown under physiologically relevant fluid shear stress conditions.

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