Inhibition of platelet binding and aggregation by streptococcal exopolysaccharide.
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.
Sullam
P M
PM
Center for Immunochemistry, VA Medical Center, San Francisco, CA 94121.
Costerton
J W
JW
Yamasaki
R
R
Dazin
P F
PF
Mills
J
J
D001792:Blood Platelets / Q000378:metabolism; D005434:Flow Cytometry; D006801:Humans; D007074:Immunoglobulin G / Q000378:metabolism; D010974:Platelet Aggregation; D011135:Polysaccharides, Bacterial / Q000096:biosynthesis / Q000502:physiology*; D013291:Streptococcus / Q000502:physiology*
D007074:Immunoglobulin G; D011135:Polysaccharides, Bacterial