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首页> 外文期刊>Infection and immunity >Multiple Functional Domains of Enterococcus faecalis Aggregation Substance Asc10 Contribute to Endocarditis Virulence
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Multiple Functional Domains of Enterococcus faecalis Aggregation Substance Asc10 Contribute to Endocarditis Virulence

机译：粪肠球菌聚集物质Asc10的多个功能域有助于心内膜炎的毒力。

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Aggregation substance proteins encoded by sex pheromone plasmids increase the virulence of Enterococcus faecalis in experimental pathogenesis models, including infectious endocarditis models. These large surface proteins may contain multiple functional domains involved in various interactions with other bacterial cells and with the mammalian host. Aggregation substance Asc10, encoded by plasmid pCF10, is induced during growth in the mammalian bloodstream, and pCF10 carriage gives E. faecalis a significant selective advantage in this environment. We employed a rabbit model to investigate the role of various functional domains of Asc10 in endocarditis. The data suggested that the bacterial load of the infected tissue was the best indicator of virulence. Isogenic strains carrying either no plasmid, wild-type pCF10, a pCF10 derivative with an in-frame deletion of the prgB gene encoding Asc10, or pCF10 derivatives expressing other alleles of prgB were examined in this model. Previously identified aggregation domains contributed to the virulence associated with the wild-type protein, and a strain expressing an Asc10 derivative in which glycine residues in two RGD motifs were changed to alanine residues showed the greatest reduction in virulence. Remarkably, this strain and the strain carrying the pCF10 derivative with the in-frame deletion of prgB were both significantly less virulent than an isogenic plasmid-free strain. The data demonstrate that multiple functional domains are important in Asc10-mediated interactions with the host during the course of experimental endocarditis and that in the absence of a functional prgB gene, pCF10 carriage is actually disadvantageous in vivo.
机译：性信息素质粒编码的聚集物质蛋白可在实验性发病机理模型（包括传染性心内膜炎模型）中提高粪肠球菌的毒性。这些大的表面蛋白可能包含多个功能域，这些功能域涉及与其他细菌细胞和哺乳动物宿主的各种相互作用。由质粒pCF10编码的聚集物质Asc10在哺乳动物血流的生长过程中被诱导，并且pCF10的运输产生了E。粪便在这种环境下具有明显的选择性优势。我们采用了兔模型来调查心内膜炎中Asc10的各种功能域的作用。数据表明感染组织的细菌载量是最好的毒力指标。不携带质粒，野生型pCF10，在编码Asc10的 prgB 基因内有框内缺失的pCF10衍生物或表达 prgB 其他等位基因的pCF10衍生物在此模型中进行了检查。先前确定的聚集域有助于与野生型蛋白相关的毒力，表达Asc10衍生物的菌株的毒力降低最大，在该菌株中，两个RGD图案中的甘氨酸残基变为丙氨酸残基。值得注意的是，该菌株和带有pCF10衍生物并带有 prgB 读框内缺失的菌株的毒力均显着低于无同基因质粒的菌株。数据表明，在实验性心内膜炎的过程中，多个功能域在Asc10介导的与宿主的相互作用中很重要，并且在缺少功能性 prgB 基因的情况下，pCF10转运在体内实际上是不利的。

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