Platelet interaction with bacteria. IV. Stimulation of the release reaction

Abstract

Release of 14C-serotonin from human platelets prelabeled with 14C-5-hydroxytryptamine was measured during platelet aggregation induced by Staphylococcus aureus. Platelet-bacteria interaction (PBI) was as potent a stimulus of the platelet release reaction as collagen, thrombin, or epinephrine. Inhibitors which blocked platelet aggregation also prevented the release reaction of PBI. Sequential measurements of release, when correlated with nephelometry of aggregation, showed close correlation between the onset of release and the onset of platelet shape change and early aggregation. Ultrastructural studies with polylysine, an agent capable of polymerizing platelet granule contents, revealed that granule components are secreted to the region of the bacteria trapped between platelets in the forming aggregates. Platelet peroxidase activity remained localized within the dense tubular system of the platelets.