Related Experiment Videos
Inhibition of platelet binding and aggregation by streptococcal exopolysaccharide
P M Sullam1, J W Costerton, R Yamasaki
1Center for Immunochemistry, VA Medical Center, San Francisco, CA 94121.
Insights
Streptococcal exopolysaccharides, key to endocarditis virulence, were found to inhibit bacterial binding and aggregation of human platelets. This suggests exopolysaccharides may limit disease progression by hindering platelet interactions.
Area of Science:
- Microbiology
- Immunology
- Pathogenesis
Background:
- Streptococcal exopolysaccharides are significant virulence factors in endocarditis.
- Bacterial adherence to heart valves and vegetation formation are promoted by these exopolysaccharides.
- Platelet interactions are hypothesized to be crucial for streptococcal endocardial colonization.
Purpose of the Study:
- To investigate the impact of streptococcal exopolysaccharides on bacterial binding to human platelets.
- To evaluate the effect of exopolysaccharides on streptococcal-induced platelet aggregation.
Main Methods:
- Flow cytometry was employed to quantify bacterial binding to platelets.
- Aggregometry was used to measure platelet aggregation induced by streptococci.
- Exopolysaccharide removal by shearing was performed to assess its role.
Main Results:
- Streptococcus salivarius strains producing minimal exopolysaccharide exhibited extensive platelet binding.
- Strains with higher exopolysaccharide production showed significantly reduced platelet binding.
- Exopolysaccharides inhibited platelet aggregation; removal restored aggregation capacity.
Conclusions:
- Streptococcal exopolysaccharides inhibit both bacterial binding to and aggregation of human platelets.
- The virulence attributed to exopolysaccharides might stem from their ability to impede platelet-mediated host interactions.
- These findings offer insights into the complex interplay between streptococci, platelets, and endocarditis pathogenesis.
Abstract:
Streptococcal exopolysaccharides are major virulence factors in the pathogenesis of endocarditis. They promote bacterial adherence to valves and subsequent vegetation formation. Since platelet binding and aggregation by streptococci are postulated mechanisms for endocardial colonization and vegetation production, the effect of exopolysaccharide on binding and aggregation was evaluated by flow cytometry and aggregometry. Streptococcus salivarius D1, a minimal exopolysaccharide producer, bound human platelets extensively (86.8% of bacteria bound by 1 min). S. Salivarius M13 and M15 and Streptococcus mitis M4 produced larger amounts of exopolysaccharide and bound platelets significantly less (52.6%, 51.2%, 52.8%, respectively). Exopolysaccharide also inhibited platelet aggregation: Strains with minimal exopolysaccharide aggregated platelets maximally, while strains with extensive exopolysaccharide failed to induce aggregation. Removal of exopolysaccharide by shearing restored aggregation by these latter strains. Thus, exopolysaccharides can inhibit the binding and aggregation of platelets by streptococci. The virulence associated with exopolysaccharide may result from the inhibition of platelet-mediated interactions that limit disease progression.