Enterococcus faecalis is a significant cause of hospital-acquired bacteremia. Herein, the discovery is reported that cardiac microlesions form during severe bacteremic E. faecalis infection in mice. The cardiac microlesions were identical in appearance to those formed by Streptococcus pneumoniae during invasive pneumococcal disease (IPD). However, E. faecalis does not encode the virulence determinants implicated in pneumococcal microlesion formation. Rather, disulfide bond forming protein DsbA was found to be required for E. faecalis virulence in a C. elegans model and was necessary for efficient cardiac microlesion formation. Furthermore, E. faecalis promoted cardiomyocyte apoptotic and necroptotic cell death at sites of microlesion formation. Additionally, loss of DsbA caused an increase in pro-inflammatory cytokines unlike the wild-type strain, which suppressed the immune response. In conclusion, we establish that E. faecalis is capable of forming cardiac microlesions and identify features of both the bacterium and the host response that are mechanistically involved.

中文翻译：

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在严重的菌血症性粪肠球菌感染期间形成心脏微损伤。

粪肠球菌是医院获得性菌血症的重要原因。在此，该发现报道了在小鼠严重菌血症性粪肠球菌感染期间形成心脏微损伤。心脏微损伤的外观与侵袭性肺炎球菌病 (IPD) 期间由肺炎链球菌形成的微损伤相同。然而，粪肠球菌不编码与肺炎球菌微损伤形成有关的毒力决定因素。相反，发现二硫键形成蛋白 DsbA 是秀丽隐杆线虫模型中粪肠球菌毒力所必需的，并且是有效心脏微损伤形成所必需的。此外，粪肠球菌促进微损伤形成部位的心肌细胞凋亡和坏死性细胞死亡。此外，与抑制免疫反应的野生型菌株不同，DsbA 的缺失导致促炎细胞因子的增加。总之，我们确定粪肠球菌能够形成心脏微损伤，并确定机械上涉及的细菌和宿主反应的特征。