AGGREGATION OF HUMAN-PLATELETS AND ADHESION OF STREPTOCOCCUS-SANGUIS
AGGREGATION OF HUMAN-PLATELETS AND ADHESION OF STREPTOCOCCUS-SANGUIS
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DOI:
10.1128/iai.39.3.1457-1469.1983
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发表时间:
1983-01-01
影响因子:
3.1
通讯作者:
CLAWSON, CC
中科院分区:
文献类型:
--
作者:
HERZBERG, MC;BRINTZENHOFE, KL;CLAWSON, CC
The hypothesis that human platelets selectively bind or adhere to strains of S. Sanguis and S. mutans and aggregate, as a result, into an in vitro thrombus was investigated. Adhesion was uncoupled from activation and aggregation by incubating streptococci with platelet ghosts in a simple, quantitative assay. Adhesion was mediated by protease-sensitive components on the streptococci and platelet ghosts rather than cell surface carbohydrates or dextrans, plasma components or divalent cations. The same streptococci were also studied by standard aggregometry techniques. Platelet-rich plasma was activated and aggregated by certain isolates of S. sanguis. Platelet ghosts bound the same strains selectively under Ca2+ and plasma-depleted conditions. Fresh platelets activated after washing; Ca2+ had to be restored. Aggregation required fresh platelets in Ca2+-restored plasma and was inducible by washed streptococcal cell walls. These reactions in the binding and aggregometry assays were confirmed by transmission EM. Surface microfibrils on intact S. sanguis were identified. These appendages bound S. sanguis to platelets. The selectivity of adhesion of the various S. sanguis strains to platelet ghosts or Ca2+- and plasma-depleted fresh washed platelets was similar for all donors. Thus, the platelet binding site was expressed widely in the population and was unlikely to be an artifact of membrane aging or preparation. Since selective adhesion of S. sanguis to platelets was apparently required for aggregation, functionally defined receptors for ligands on certain strains of S. sanguis may be present on human platelets. Some differences in the selectivity and rate of the aggregation response were noted among platelet donors; the meaning of the variability requires further study. These interactions may contribute to platelet accretion in the initiation and development of vegetative lesions in subacute bacterial endocarditis.