Platelet Aggregation Induced by Serotype Polysaccharides fromStreptococcus mutans
| Autor: | Jen-Yang Chen, Huei-Ting Lien, Jean-San Chia, Ya-Lin Lin |
|---|---|
| Rok vydání: | 2004 |
| Předmět: |
Blood Platelets
Platelet Aggregation Immunology Prostaglandin In Vitro Techniques Biology Microbiology Bacterial cell structure Immunoglobulin G Flow cytometry Streptococcus mutans Cell wall chemistry.chemical_compound Streptococcal Infections medicine Animals Humans Platelet Serotyping Cell Size Cellular Microbiology: Pathogen-Host Cell Molecular Interactions medicine.diagnostic_test Polysaccharides Bacterial Endocarditis Bacterial biology.organism_classification Antibodies Bacterial In vitro Infectious Diseases chemistry Biochemistry biology.protein Biophysics Parasitology Rabbits |
| Zdroj: | Infection and Immunity. 72:2605-2617 |
| ISSN: | 1098-5522 0019-9567 |
| Popis: | Platelet aggregation plays an important role in the pathogenesis of infective endocarditis induced by viridans streptococci or staphylococci. Aggregation induced in vitro involves direct binding of bacteria to platelets through multiple surface components. Using platelet aggregometry, we demonstrated in this study that twoStreptococcus mutanslaboratory strains, GS-5 and Xc, and two clinical isolates could aggregate platelets in an irreversible manner in rabbit platelet-rich plasma preparations. The aggregation was partially inhibited by prostaglandin I2(PGI2) in a dose-dependent manner. Whole bacteria and heated bacterial cell wall extracts were able to induce aggregation. Cell wall polysaccharides extracted from the wild-type Xc strain, containing serotype-specific polysaccharides which are composed of rhamnose-glucose polymers (RGPs), could induce platelet aggregation in the presence of plasma. Aggregation induced by the serotype-specific RGP-deficient mutant Xc24R was reduced by 50% compared to the wild-type strain Xc. In addition, cell wall polysaccharides extracted from Xc24R failed to induce platelet aggregation. The Xc strain, but not the Xc24R mutant, could induce platelet aggregation when preincubated with plasma. Both Xc and Xc24R failed to induce platelets to aggregate in plasma depleted of immunoglobulin G (IgG), but aggregation was restored by replenishment of anti-serotype c IgG. Analysis by flow cytometry showed thatS. mutansRGPs could bind directly to rabbit and human platelets. Furthermore, cell wall polysaccharides extracted from the Xc, but not the Xc24R, strain could induce pseudopod formation of both rabbit and human platelets in the absence of plasma. Distinct from the aggregation of rabbit platelets, bacterium-triggered aggregation of human platelets required a prolonged lag phase and could be blocked completely by PGI2. RGPs also trigger aggregation of human platelets in a donor-dependent manner, either as a transient and reversible or a complete and irreversible response. These results indicated that serotype-specific RGPs, a soluble product ofS. mutans, could directly bind to and activate platelets from both rabbit and human. In the presence of plasma containing IgG specific to RGPs, RGPs could trigger aggregation of both human and rabbit platelets, but the degree of aggregation in human platelets depends on the donors. |
| Databáze: | OpenAIRE |
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