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Infection and Immunity, August 2000, p. 4699-4705, Vol. 68, No. 8
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Influence of Platelets and Platelet Microbicidal Protein Susceptibility on the Fate of Staphylococcus aureus in an In Vitro Model of Infective Endocarditis

Renee-Claude Mercier,1,2,* Michael J. Rybak,1,3 Arnold S. Bayer,4,5 and Michael R. Yeaman4,5

The Anti-Infective Research Laboratory, Detroit Receiving Hospital/University Health Center and College of Pharmacy,1 and Department of Internal Medicine, School of Medicine, Wayne State University,3 Detroit, Michigan 48201; University of New Mexico-College of Pharmacy, Albuquerque, New Mexico 871312; Department of Medicine, Division of Infectious Diseases, St. John's Cardiovascular Research Center, LAC-Harbor UCLA Medical Center Research and Education Institute, Torrance, California 905024; and School of Medicine, University of California, Los Angeles, California 900245

Received 16 March 2000/Returned for modification 27 April 2000/Accepted 15 May 2000

Several lines of evidence indicate that platelets protect against endovascular infections such as infective endocarditis (IE). It is highly likely that a principal mechanism of this platelet host defense role is the release of platelet microbicidal proteins (PMPs) in response to agonists generated at sites of endovascular infection. We studied the ability of platelets to limit the colonization and proliferation of Staphylococcus aureus in an in vitro model of IE. Three isogenic S. aureus strains, differing in their in vitro susceptibility to thrombin-induced platelet microbicidal protein-1 (tPMP), were used: ISP479C (parental strain; highly susceptible to tPMP [tPMPs]); ISP479R (transposon mutant derived from ISP479; tPMP resistant [tPMPr]); or 757-5 (tPMPr transductant of the ISP479R genotype in the ISP479 parental background). Time-kill assays and in vitro IE models were used to examine the temporal relationship between thrombin-induced platelet activation and S. aureus killing. In time-kill studies, early platelet activation (30 min prior to bacterial exposure) correlated with a significant bactericidal effect against tPMPs ISP479C (r2 > 0.90, P < 0.02) but not against tPMPr strains, ISP479R or 757-5. In the IE model, thrombin activation significantly inhibited proliferation of ISP479C within simulated vegetations compared to strains ISP479R or 757-5 (P < 0.05). The latter differences were observed despite there being no detectable differences among the three S. aureus strains in initial colonization of simulated vegetations. Collectively, these data indicate that platelets limit intravegetation proliferation of tPMPs but not tPMPr S. aureus. These findings underscore the likelihood that platelets play an important antimicrobial host defense role in preventing and/or limiting endovascular infections due to tPMPs pathogens.

* Corresponding author. Mailing address: University of New Mexico/College of Pharmacy, 2502 Marble NE, Albuquerque, NM 87131. Phone: (505) 272-0581. Fax: (505) 272-6749. E-mail: rmercier{at}unm.edu.

Infection and Immunity, August 2000, p. 4699-4705, Vol. 68, No. 8
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


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