Platelet aggregation by group B streptococci.
Forty-six strains of group B streptococci (GBS), including various serotypes and non-serotypable strains, were tested for their ability to induce platelet aggregation in human platelet-rich plasma; four strains, all belonging to type III, showed a positive reaction. The characteristics of the reaction were investigated in these four positive strains. Aggregation was dependent on the ratio of bacteria to platelets, being maximal at a ratio of 4.3. Platelet aggregation was inhibited by EDTA (100% inhibition at 3.1 mM), indomethacin (100% inhibition at 10 mM), acetylsalicylic acid (93-100% inhibition at 5.0 mM) and quinacrine (100% inhibition at 0.25 mM). Thus the reaction was cation-dependent and required cyclooxygenase activity. Assays for cytosolic lactate dehydrogenase did not indicate platelet lysis. GBS induced the release of [3H]serotonin, which was maximal (68-78%) at 10 min after the reaction was started. Experiments with gel-filtered platelets suggested that GBS-induced platelet aggregation required both fibrinogen and heat-resistant (56 degrees C, 30 min) serum factors. Type-specific antisera prevented the platelet aggregation activity of heat-killed bacteria, but not of live bacteria. Trypsin digestion of the bacterial cells caused an almost complete loss of the platelet aggregation activity.
D001241:Aspirin / Q000494:pharmacology; D001792:Blood Platelets / Q000378:metabolism; D004492:Edetic Acid / Q000494:pharmacology; D006801:Humans; D007213:Indomethacin / Q000494:pharmacology; D007770:L-Lactate Dehydrogenase / Q000096:biosynthesis; D010974:Platelet Aggregation / Q000187:drug effects; D010976:Platelet Count; D011796:Quinacrine / Q000494:pharmacology; D012701:Serotonin / Q000096:biosynthesis; D013292:Streptococcus agalactiae / Q000276:immunology*
D012701:Serotonin; D004492:Edetic Acid; D007770:L-Lactate Dehydrogenase; D011796:Quinacrine; D001241:Aspirin; D007213:Indomethacin