Bacteria stimulate platelet aggregation and secretion in plasma. (A) Characterization of the lag time for onset of aggregation in response to bacteria. Platelet aggregation in response to bacterial strains belonging to 5 different gram-positive species was monitored in plasma by light transmission aggregometry. Final concentrations of bacteria were S sanguinis 133-79, 0.6 × 108 CFU/mL; S aureus Newman, 1 × 108 CFU/mL; S gordonii DL1, 3 × 108 CFU/mL; S oralis CR834, 4 × 108 CFU/mL; S pneumoniae IO1196, 0.7 × 108 CFU/mL. Results are shown as mean ± SD of 4 independent experiments. (B) Effect of αIIbβ3 inhibitor Integrilin on platelet dense granule secretion in response to bacteria. Aggregation reactions were performed in plasma in the presence of Integrilin (9 μM) or vehicle; supernatants collected at time of full aggregation, or a parallel time point in the case of inhibition. Supernatants were analyzed for ATP release by luciferin-luciferase assay. ATP levels released in 32 μM TRAP-stimulated platelets were used to normalize data. Results are shown as mean ± SD of 4 independent experiments; *P < .05. (C) Effect of αIIbβ3 inhibitor Integrilin on platelet PF4 release in response to bacteria. Aggregation reactions were performed in plasma in the presence of Integrilin (9 μM) or vehicle and supernatants collected at time of full aggregation, or a parallel time point in the case of inhibition. Levels of soluble PF4 were measured in duplicates by PF4 ELISA. Results are shown as mean ± SD of 4 independent experiments; *P < .05.
