Summary

There is increasing evidence for a relationship between bacterialinfections and several cardiovascular disorders.Although theprecise mechanism(s) underlying this association is unknown,the direct activation of platelets by bacteria is one possibility. Individualstrains of S. sanguis activate platelets in a non-uniform,donor-dependent manner. In the current study, platelet aggregationprofiles were obtained for fourteen donors in responseto four strains of S. sanguis (2017–78, 133–79, SK112, SK108a)and one of S. gordonii (SK8) . The platelets from all donors respondedto strains 2017–78 and 133–79,whereas strains SK112,SK8 and SK108a caused aggregation in one, five and twelve donors,respectively. Immunoglobulin G (IgG) binding to strains 2017–78, 133–79 and SK108a were significantly greater than tostrains SK112 and SK8. Absorption of IgG by strain 2017–78caused significant decreases in IgG binding, and platelet aggregationin response, to all strains. Single-strand conformationalpolymorphisms were observed in the Fc? RIIA gene from fourdonors. Sequencing revealed two known and two novel pointmutations, none of which correlated with the aggregation profile.Thus, platelet activation to the various strains depends on acommon IgG and, while in most cases the level of IgG binding toS. sanguis determines platelet responsiveness, neither the levelsof IgG nor Fc? RIIA polymorphisms can fully account for donorvariability.