1178 TYPE SPECIFIC ANTIBODY PREVENTS PLATELET AGGREGATION INDUCED BY GROUP B STREPTOCOCCUS TYPE III

Abstract

Group B streptococcus type III (GBS III) organisms readily induce platelet aggregation and serotonin release in human platelet rich plasma (PRP). In a system employing 108 platelets in PRP and 106–108 live GBS III, aggregation usually occurred after 3–7 minutes incubation. Serotonin release began within the first minute and usually reached about 40% before aggregation was detected. The addition of type specific rabbit antisera inhibited aggregation and release in a dose dependent fashion, but rabbit antisera against GBS type II and pneumococcus types 14 and 19 had no effect. To test the activity of different isotypes, monoclonal antibodies against the sialic acid determinant of the GBS III antigen were used. IgG, IgM, and IgA antibodies were all effective in blocking aggregation and release. While the significance of this phenomenon is not clear, it may represent a protective function of antibody which is not directly related to opsonization and phagocytosis. If type specific antibody prevented release of platelet activators in vivo this could affect the hemodynamic changes, especially pulmonary hypertension, often seen in GBS sepsis and in animal models of the GBS sepsis syndrome.