作者: Jean-San Chia , Ya-Lin Lin , Huei-Ting Lien , Jen-Yang Chen
DOI: 10.1128/IAI.72.5.2605-2617.2004
关键词:
摘要: Platelet aggregation plays an important role in the pathogenesis of infective endocarditis induced by viridans streptococci or staphylococci. Aggregation vitro involves direct binding bacteria to platelets through multiple surface components. Using platelet aggregometry, we demonstrated this study that two Streptococcus mutans laboratory strains, GS-5 and Xc, clinical isolates could aggregate irreversible manner rabbit platelet-rich plasma preparations. The was partially inhibited prostaglandin I2 (PGI2) a dose-dependent manner. Whole heated bacterial cell wall extracts were able induce aggregation. Cell polysaccharides extracted from wild-type Xc strain, containing serotype-specific which are composed rhamnose-glucose polymers (RGPs), presence plasma. RGP-deficient mutant Xc24R reduced 50% compared strain Xc. In addition, failed but not mutant, when preincubated with Both depleted immunoglobulin G (IgG), restored replenishment anti-serotype c IgG. Analysis flow cytometry showed S. RGPs bind directly human platelets. Furthermore, Xc24R, pseudopod formation both absence Distinct platelets, bacterium-triggered required prolonged lag phase be blocked completely PGI2. also trigger donor-dependent manner, either as transient reversible complete response. These results indicated RGPs, soluble product mutans, activate human. IgG specific degree depends on donors.