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Clumping factor A mediates binding of Staphylococcus aureus to human platelets
I R Siboo1, A L Cheung, A S Bayer
1Veterans Affairs Medical Center and University of California San Francisco, San Francisco, California, USA.
Infection and Immunity
|April 9, 2001
Summary
Staphylococcus aureus binding to platelets is key in infective endocarditis. The clumping factor A (ClfA) protein mediates this interaction by binding to a novel 118-kDa platelet receptor, impacting bacterial virulence.
Area of Science:
- Microbiology
- Immunology
- Infectious Diseases
Background:
- Bacterial adherence to platelets is a critical virulence factor in infective endocarditis pathogenesis.
- Staphylococcus aureus strain PS12, a mutant with reduced platelet binding, exhibits lower virulence in animal models.
Purpose of the Study:
- To characterize the gene disrupted in S. aureus strain PS12 and elucidate its role in platelet binding.
- To identify the specific bacterial and host factors involved in S. aureus-platelet interactions.
Main Methods:
- Genetic analysis (DNA sequencing, Southern blotting, PCR) to identify Tn551 insertion sites within the clumping factor A (ClfA) locus.
- Production and purification of recombinant ClfA A region for in vitro binding assays.
- Immunoprecipitation assays to identify platelet binding partners of ClfA.
Main Results:
- Tn551 insertions in PS12 disrupted the clfA gene, leading to a truncated, secreted ClfA protein.
- Recombinant ClfA A region significantly inhibited S. aureus binding to human platelets.
- ClfA directly bound to a novel 118-kDa platelet membrane protein, distinct from glycoprotein IIb.
Conclusions:
- The clumping factor A (ClfA) of Staphylococcus aureus is a key mediator of direct platelet binding.
- This interaction involves a novel 118-kDa platelet membrane receptor, contributing to S. aureus virulence in infective endocarditis.