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Infect. Immun. doi:10.1128/IAI.01993-06
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

Both complement- and fibrinogen-dependent mechanisms contribute to platelet aggregation mediated by Staphylococcus aureus Clumping factor B

Department of Microbiology, Moyne Institute of Preventive Medicine, Trinity College Dublin 2, Ireland; and Department of Clinical Pharmacology, Royal College of Surgeons in Ireland, Dublin 2, Ireland

^* To whom correspondence should be addressed. Email: tfoster{at}tcd.ie.

	Abstract

Staphylococcus aureus can stimulate activation and aggregation of platelets which is thought to be a factor in the development of infective endocarditis. Previous studies have identified Clumping factor A and the Fibronectin binding proteins A and B as potent platelet aggregators. These proteins are able to stimulate rapid platelet aggregation by either a fibrinogen or fibronectin dependent process which also requires antibodies specific to each protein. Slower aggregation has been seen in other systems where specific fibrinogen binding ligands are absent and platelet aggregation is mediated by complement and specific antibodies.

Bacteria expressing clumping factor B (ClfB) aggregate platelets with a longer lag time than ClfA or FnBPA and FnBPB. In order to investigate whether ClfB causes platelet aggregation in a complement- or fibrinogen-dependent manner a non-fibrinogen binding mutant of ClfB (ClfB Q235A) was constructed. L. lactis expressing ClfB Q235A was able to stimulate platelet aggregation in platelet rich plasma without a significant increase in lag time. The requirements for platelet aggregation were investigated using gel filtered platelets. Fibrinogen and specific anti-ClfB antibodies were found to be sufficient to allow platelet aggregation mediated by the wild type ClfB protein. It seems that ClfB causes platelet aggregation by a fibrinogen dependent mechanism. The non- fibrinogen binding ClfB mutant was unable to stimulate platelet aggregation under these conditions. However bacteria expressing ClfB Q235A caused platelet aggregation in a complement- dependent manner which required specific anti-ClfB antibodies.

This article has been cited by other articles:

• Walsh, E. J., Miajlovic, H., Gorkun, O. V., Foster, T. J. (2008). Identification of the Staphylococcus aureus MSCRAMM clumping factor B (ClfB) binding site in the {alpha}C-domain of human fibrinogen. Microbiology 154: 550-558 [Abstract] [Full Text]