Staphylococcus aureus fibronectin-binding protein (FnBP)-mediated adherence to platelets, and aggregation of platelets induced by FnBPA but not by FnBPB.

BACKGROUND

The ability of Staphylococcus aureus to adhere to platelets and to induce aggregation of platelets is considered to be a critical factor in S. aureus-associated infective endocarditis.

METHODS

To identify and characterize further bacterial factors involved in the S. aureus-platelet interaction, we generated a phage-display library of S. aureus genomic DNA by use of the improved phagemid vector pG8SAET. The library was affinity-panned against gel-filtered, immobilized platelets.

RESULTS

Repeatedly isolated clones contained overlapping DNA fragments encoding a portion of the S. aureus fibronectin (Fn)-binding proteins (FnBPs). In a flow cytometric adherence assay, Staphylococcus carnosus that heterologously expressed either fnbA or fnbB, which encode FnBPA and FnBPB, respectively, showed increased adherence to activated, gel-filtered platelets. Adherence was promoted by the addition of Fn or fibrinogen (Fg), which most likely act as bridging molecules. Interestingly, promotion of adherence mediated by Fn was in the same range with S. carnosus producing either FnBPA or FnBPB, whereas promotion of adherence mediated by Fg was significantly more pronounced with S. carnosus that produce FnBPA than with S. carnosus that produce FnBPB. Furthermore, FnBPA, but not FnBPB, mediated aggregation of platelets when present on S. carnosus cells.

CONCLUSION

Our results indicate a substantial functional difference between FnBPA and FnBPB in the S. aureus-platelet interaction.