Enterococci-induced platelet aggregation is an ion-dependent, cyclooxygenase-insensitive process requiring plasma components.
Ion-dependent enterococcal platelet activation merits human mechanistic studies; leaves open any role in clinical thrombosis or endocarditis.
The platelet aggregation capability of whole cells of Enterococcus faecalis, E. faecium and E. avium was tested. The optimum ratios of bacteria to platelets in E. faecalis (strain SMU-37), E. faecium (strain SMU-138) and E. avium (strain SMU-197) were 1.0, 1.2 and 2.0, respectively. During the platelet aggregation induced by the three strains of enterococci, 65-69% of total serotonin was released. The aggregation was totally inhibited by ethylenediaminetetraacetate (10 mM) and apyrase (1 mg/ml), while no effect was shown by aspirin (10 mM), indomethacin (10 mM) and quinacrine (1 mM). By pretreatment of platelet-poor plasma with heat (56 C, 30 min) or zymosan, the reactivities with platelets of each strain of species were markedly diminished. These results suggest that enterococci-induced platelet aggregation was an ion-dependent, cyclooxygenase-insensitive event, and plasma component(s) was (were) required for the reaction.
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Usui et al. (1991) studied this question.
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