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Infect. Immun. doi:10.1128/IAI.00909-07
Copyright (c) 2007, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

The Role of Streptococcus gordonii Surface Proteins SspA/B and Hsa in Platelet Function

Molecular and Cellular Therapeutics, Royal College of Surgeons in Ireland, Dublin 2, Ireland; Department of Oral and Dental Science, University of Bristol, Bristol BS1 2LY, United Kingdom; School of Medicine & Medical Science, Conway Institute for Biomolecular & Biomedical Sciences, University College Dublin, Dublin 4, Ireland

^* To whom correspondence should be addressed. Email: skerrigan{at}rcsi.ie.

	Abstract

Streptococcus gordonii colonization of damaged heart surfaces in infective endocarditis is dependent upon the recognition of host receptors by specific bacterial surface proteins. However, despite several attempts to identify the mechanisms involved in this interaction, the nature of the bacterial proteins required remains poorly understood. This study provides clear evidence that several S. gordonii surface proteins participate in the interaction with platelets to support platelet adhesion and induce platelet aggregation. S. gordonii strains were found to support strong (DL1-Challis, SK12, SK184 and Blackburn) or moderate (UB1545 hsa and CH1-Challis) adhesion, or failed to support platelet adhesion (M5, M99 and Channon). In addition, under flow conditions, platelets rolled and subsequently adhered to immobilized S. gordonii at low shear (50 s^-1) in a Hsa-dependent manner but did not interact with S. gordonii DL1 at any shear rate >50 s^-1. S. gordonii strains either induced (DL1-Challis, SK12, SK184, UB1545 hsa and M99) or failed to induce (M5, CH1-Challis, Channon and Blackburn) platelet aggregation. Using a proteomic approach to identify differential cell wall protein expression between aggregating (DL1) and non-aggregating (Blackburn) strains we identified Antigen I/II family proteins SspA and SspB. Over expression of SspA or SspB in the platelet non-reactive L. lactis induced GPIIb/IIIa-dependent platelet aggregation similar to that seen with S. gordonii DL1. However, they failed to support platelet adhesion. Thus, S. gordonii has distinct mechanisms for supporting platelet adhesion and inducing platelet aggregation. Differential protein expression between strains may be important in the pathogenesis of invasive diseases such as infective endocarditis.