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CcpA Is Important for Growth and Virulence of Enterococcus faecium

机译：CcpA对粪肠球菌的生长和毒力很重要

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The collagen adhesin Acm was the first virulence determinant reported to be important for the pathogenesis of Enterococcus faecium in a rat infective endocarditis model. We had previously reported that there was a slight growth delay associated with acm allelic replacement (cat) mutant strain TX6051 used in that study. Recently, we generated a nonpolar markerless acm deletion mutant and did not observe a delay in growth. We therefore performed comparative genome sequence analysis of wild-type strain TX82 and TX6051 and found a single mutation, a nonsense mutation in the ccpA gene of TX6051. After correcting this mutation, the growth defect of TX6051 was abolished, implicating a role for CcpA in the growth of E. faecium. To confirm this, we created a ccpA deletion mutant of TX82, which also exhibited a slight delay in growth. Furthermore, the ccpA deletion mutant was attenuated (P = 0.0024) in a mixed-inoculum (TX82 plus TX82 ΔccpA) rat endocarditis model and also in an in vitro competitive growth assay; a ccpA-complemented strain showed neither reduced growth nor reduced virulence. We also found attenuation in the endocarditis model with the new acm deletion mutant although not as great as that previously observed with TX6051 carrying the ccpA mutation. Taken together, our data confirm the role of Acm in the pathogenesis of endocarditis. We also show that CcpA affects the growth of E. faecium, that an intact ccpA gene is important for full virulence, and that a ccpA mutation was partly responsible for the highly attenuated phenotype of TX6051.
机译：在大鼠感染性心内膜炎模型中，胶原粘附素Acm是第一个对粪便肠球菌的发病机理重要的毒力决定因素。我们之前曾报道过，该研究中使用的acm等位基因替换（猫）突变体菌株TX6051有轻微的生长延迟。最近，我们生成了一个非极性的无标记Acm缺失突变体，并且未观察到生长延迟。因此，我们对野生型菌株TX82和TX6051进行了比较的基因组序列分析，发现TX6051的ccpA基因中有一个单一的突变，即无意义的突变。纠正此突变后，TX6051的生长缺陷被消除，这暗示了CcpA在屎肠球菌的生长中的作用。为了证实这一点，我们创建了TX82的ccpA缺失突变体，该突变体还显示出生长的轻微延迟。此外，在混合接种物（TX82加TX82ΔccpA）大鼠心内膜炎模型以及体外竞争性生长试验中，ccpA缺失突变体减毒（P = 0.0024）。 ccpA互补菌株既没有显示出生长减少，也没有显示出毒性。我们还发现了新的acm缺失突变体在心内膜炎模型中的衰减，尽管不如先前携带ccpA突变的TX6051所观察到的衰减大。综上所述，我们的数据证实了Acm在心内膜炎的发病机理中的作用。我们还显示，CcpA影响屎肠球菌的生长，完整的ccpA基因对于充分的毒力很重要，并且ccpA突变部分负责TX6051的高度减毒表型。

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