变形链球菌细胞表面蛋白抗原c对血小板聚集的贡献。

M Matsumoto-Nakano, M Tsuji, S Inagaki, K Fujita, K Nagayama, R Nomura, T Ooshima
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引用次数: 23

摘要

简介:变形链球菌被认为是引起感染性心内膜炎的病原体之一。本研究的目的是通过关注其高分子蛋白抗原c (PAc)来研究变形链球菌在血小板聚集方面的特性。方法:采用聚集仪和共聚焦显微镜对6株临床株和1株等基因突变株的血小板聚集特性进行分析,并采用抗pac血清对血小板聚集进行抑制试验。结果:表达PAc的S. mutans菌株诱导血小板聚集,而PAc缺陷突变株和两株不表达PAc的临床分离株则没有。当用较高剂量的抗PAc血清预处理血小板时,血小板聚集率呈剂量依赖性降低,表明PAc直接与血小板结合。结论:变形链球菌PAc参与人血小板聚集,可能是感染性心内膜炎发病的毒力因素之一。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Contribution of cell surface protein antigen c of Streptococcus mutans to platelet aggregation.

Introduction: Streptococcus mutans is considered to be one of the pathogens that cause infective endocarditis. The purpose of the present study was to examine the properties of S. mutans with regard to platelet aggregation by focusing on its high molecular protein antigen c (PAc).

Methods: The platelet aggregation properties of six clinical strains and one isogenic mutant strain of S. mutans were analysed using an aggregometer and confocal microscopy, as well as with an inhibition assay of platelet aggregation using anti-PAc serum.

Results: S. mutans strains with PAc expression induced platelet aggregation, while a PAc-deficient mutant and two clinical isolates with no PAc expression did not. When platelets were pretreated with higher amounts of anti-PAc serum, the platelet aggregation rate was reduced in a dose-dependent manner, indicating that PAc binds directly to platelets.

Conclusion: S. mutans PAc is involved in human platelet aggregation and may be one of the virulence factors in the pathogenesis of infective endocarditis.

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