Yazarlar : Claes J1, Vanassche T1, Peetermans M

Yayın : Blood.

Yayın Yılı : 2014

Pubmed Linki : http://www.ncbi.nlm.nih.gov/pubmed/24951431

Konu : Tromboz

Literatür İçeriği :  Adhesion of Staphylococcus aureus (S. aureus) to blood vessels under shear stress requires von Willebrand factor (VWF). Several bacterial factors have been proposed to interact with VWF, including von Willebrand factor-binding protein (vWbp), a secreted coagulase that activates the host's prothrombin to generate fibrin. We measured the adhesion of S. aureus Newman and a vWbp-deficient mutant (vwb) to VWF, collagen, and activated endothelial cells in a micro-parallel flow chamber. In vivo adhesion of S. aureus was evaluated in the mesenteric circulation of wildtype and VWF-deficient mice. We found a shear-dependent increase in adhesion of S. aureus to the (sub)endothelium that was dependent on interactions between vWbp and the A1-domain of VWF. Adhesion was further enhanced by coagulase-mediated fibrin formation that clustered bacteria and recruited platelets into bacterial microthrombi. In vivo, deficiency of vWbp or VWF as well as inhibition of coagulase activity reduced S. aureus adhesion. We conclude that vWbp contributes to vascular adhesion of S. aureus through two independent mechanisms: shear-mediated binding to VWF and activation of prothrombin to form S. aureus-fibrin-platelet aggregates.

Copyright © 2014 American Society of Hematology.

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