These authors contributed equally to this work.
Staphylococcal superantigen-like 5 activates platelets and supports platelet adhesion under flow conditions, which involves glycoprotein Ibα and αIIbβ3
Version of Record online: 28 JUL 2009
© 2009 International Society on Thrombosis and Haemostasis
Journal of Thrombosis and Haemostasis
Volume 7, Issue 11, pages 1867–1874, November 2009
How to Cite
DE HAAS, C. J. C., WEETERINGS, C., VUGHS, M. M., DE GROOT, P. G., VAN STRIJP, J. A. and LISMAN, T. (2009), Staphylococcal superantigen-like 5 activates platelets and supports platelet adhesion under flow conditions, which involves glycoprotein Ibα and αIIbβ3. Journal of Thrombosis and Haemostasis, 7: 1867–1874. doi: 10.1111/j.1538-7836.2009.03564.x
- Issue online: 21 OCT 2009
- Version of Record online: 28 JUL 2009
- Received 24 February 2009, accepted 9 July 2009
- flow conditions;
- S. aureus;
Summary. Objectives: Staphylococcal superantigen-like 5 (SSL5) is an exoprotein secreted by Staphylococcus aureus that has been shown to inhibit neutrophil rolling over activated endothelial cells via a direct interaction with P-selectin glycoprotein ligand 1 (PSGL-1). Methods and Results: When purified recombinant SSL5 was added to washed platelets in an aggregometry set-up, complete and irreversible aggregation was observed. Proteolysis of the extracellular part of GPIbα or the addition of dRGDW abrogated platelet aggregation. When a mixture of isolated platelets and red cells was perfused over immobilized SSL5 at a shear rate of 300 s−1, stable platelet aggregates were observed, and platelet deposition was substantially reduced after proteolysis of GPIb or after addition of dRGDW. SSL5 was shown to interact with glycocalicin, a soluble GPIbα fragment, and binding of SSL5 to platelets resulted in GPIb-mediated signal transduction as evidenced by translocation of 14-3-3ζ. In addition, SSL5 was shown to interact with endothelial cell matrix (ECM) and this interaction enhanced aggregation of platelets from whole blood to this ECM. Conclusions: SSL5 activates and aggregates platelets in a GPIbα-dependent manner, which could be important in colonization of the vascular bed and evasion of the immune system by S. aureus.