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首页> 外文期刊>Infection and immunity >FimA, a major virulence factor associated with Streptococcus parasanguis endocarditis.
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FimA, a major virulence factor associated with Streptococcus parasanguis endocarditis.

机译：FimA，一种与副链球菌心内膜炎相关的主要毒力因子。

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Adherence of microorganisms to damaged heart tissue is a crucial event in the pathogenesis of infective endocarditis. In the present study, we investigated the role of the FimA protein as a potential virulence factor associated with Streptococcus parasanguis endocarditis. FimA is a 36-kDa surface protein that is a recognized adhesin in the oral cavity where it mediates adherence to the salivary pellicle. An insertion mutant and a deletion mutant of S. parasanguis were employed in the rat model of endocarditis to determine the relevance of FimA in endocarditis pathogenesis. Catheterized rats were infected with either the fimA deletion mutant VT929, the fimA insertion mutant VT930, or the isogenic, wild-type S. parasanguis FW213. Rats inoculated with FW213 developed endocarditis more frequently (50.9%) than animals inoculated with either the deletion mutant (2.7%) or the insertion mutant (7.6%) (P < 0.001). A series of in vitro assays were performed to explore the mechanism(s) by which FimA enhanced the infectivity of S. parasanguis. FimA did not inhibit the uptake or the subsequent killing of S. parasanguis by phagocytic granulocytes. Similarly, FimA did not play a role in the adherence to or the aggregation of platelets. Significant differences were noted between FW213 and VT929 (P < 0.05) and FW213 and VT930 (P < 0.001) in their abilities to bind to fibrin monolayers. The mean percent adherence of FW213 to fibrin monolayers (2.1%) was greater than those of VT929 (0.5%) and VT930 (0.12%). Taken together, these results indicate that FimA is a major virulence determinant associated with S. parasanguis endocarditis and further suggest that its role is associated with initial colonization of damaged heart tissue.
机译：微生物对受损心脏组织的粘附是感染性心内膜炎发病机理中的关键事件。在本研究中，我们调查了FimA蛋白作为副血链球菌心内膜炎相关的潜在毒力因子的作用。 FimA是一种36 kDa的表面蛋白，是口腔中公认的粘附素，可介导粘附到唾液薄膜上。在心内膜炎的大鼠模型中使用了副糖链霉菌的插入突变体和缺失突变体，以确定FimA与心内膜炎发病机理的相关性。插入导管的大鼠感染了fimA缺失突变体VT929，fimA插入突变体VT930或同基因的野生型副乳链球菌FW213。接种FW213的大鼠比接种缺失突变体（2.7％）或插入突变体（7.6％）的动物发生心内膜炎的频率更高（50.9％）（P <0.001）。进行了一系列体外测定，以探索FimA增强副血链球菌感染性的机制。 FimA没有抑制吞噬粒细胞对副血吸虫的摄取或随后的杀死。同样，FimA在血小板的粘附或聚集中也不起作用。 FW213和VT929之间的显着差异（P <0.05）和FW213和VT930之间的显着差异（P <0.001）。 FW213对纤维蛋白单层的平均粘附百分比（2.1％）大于VT929（0.5％）和VT930（0.12％）。综上所述，这些结果表明FimA是与副伤寒沙门氏菌心内膜炎相关的主要毒力决定因素，并且进一步表明其作用与受损心脏组织的最初定植有关。

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