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Type-specific antibody prevents platelet aggregation induced by group B streptococci type III
The Journal of Laboratory and Clinical Medicine
|April 1, 1986
Summary
Group B streptococci (GBS) type III induced platelet aggregation and serotonin release. Antibodies effectively blocked these responses, suggesting a non-opsonic protective role.
Area of Science:
- Microbiology
- Immunology
- Hematology
Background:
- Group B streptococci (GBS) are a significant cause of neonatal infections.
- GBS type III is a prevalent serotype associated with invasive disease.
- The interaction between GBS and human platelets is not fully understood.
Purpose of the Study:
- To investigate the effect of GBS type III on human platelet function.
- To determine the role of specific antibodies in modulating GBS-induced platelet responses.
Main Methods:
- Human platelet-rich plasma (PRP) was incubated with GBS type III.
- Platelet aggregation and serotonin release were measured.
- The effects of type-specific antisera and monoclonal antibodies (IgG, IgM, IgA) were assessed.
Main Results:
- GBS type III readily induced platelet aggregation and serotonin release in PRP.
- Aggregation occurred within minutes, with significant serotonin release preceding it.
- Type-specific rabbit antisera against GBS type III inhibited these responses in a dose-dependent manner.
- Monoclonal antibodies of IgG, IgM, and IgA isotypes effectively blocked GBS-induced platelet activation.
Conclusions:
- GBS type III actively modulates human platelet function, inducing aggregation and serotonin release.
- Antibodies against GBS type III antigens can inhibit these platelet responses.
- This antibody-mediated inhibition may represent a novel protective mechanism beyond opsonization and phagocytosis.