Platelet aggregation by Streptococcus pyogenes.
Heat-killed group A Streptococcus pyogenes induced platelet aggregation in platelet-rich plasma. Aggregation was dependent upon the ratio of platelets to bacteria, with maximal aggregation occurring at 0.8 platelets per bacterium (final concentration, 300,000 per microliter). Inhibition of the reaction by 3 mM EDTA indicated it was a true aggregation and not merely adhesion and agglutination. Lactic acid dehydrogenase assays indicated lysis of platelets did not occur during a 6-min incubation period. Aggregation was inhibited in a dose-dependent manner by acetylsalicylic acid (100 microM to 10 mM) and quinacrine (15.6 to 250 microM), with no decrease in aggregation at the lowest concentration of inhibitor tested. S. pyogenes induced the release of [14C]serotonin, which was maximal (50%) at 2.4 min, when aggregation was nearly complete. Gel-filtered platelets were not aggregated unless fibrinogen (final concentration, 1.8 mg/ml) was included in the reaction mixture. Staphylococcus aureus, a group B streptococcus, and Escherichia coli were unable to induce aggregation in platelet-rich plasma under the conditions used for S. pyogenes.
D001241:Aspirin / Q000494:pharmacology; D001792:Blood Platelets / Q000378:metabolism; D004492:Edetic Acid / Q000494:pharmacology; D004926:Escherichia coli / Q000502:physiology; D005340:Fibrinogen / Q000494:pharmacology; D006801:Humans; D010974:Platelet Aggregation / Q000187:drug effects; D011796:Quinacrine / Q000494:pharmacology; D012701:Serotonin / Q000378:metabolism; D013211:Staphylococcus aureus / Q000502:physiology; D013292:Streptococcus agalactiae / Q000502:physiology; D013297:Streptococcus pyogenes / Q000502:physiology*
D012701:Serotonin; D005340:Fibrinogen; D004492:Edetic Acid; D011796:Quinacrine; D001241:Aspirin