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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >A eukaryotic-type Ser/Thr kinase in Enterococcus faecalis mediates antimicrobial resistance and intestinal persistence
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A eukaryotic-type Ser/Thr kinase in Enterococcus faecalis mediates antimicrobial resistance and intestinal persistence

机译：粪肠球菌中的真核型Ser / Thr激酶介导抗菌素耐药性和肠道持久性

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摘要

Antibiotic-resistant enterococci are major causes of hospital-acquired infections. The emergence of Enterococcus faecalis as a significant nosocomial pathogen is a consequence of its inherent resistance to certain antibiotics and of its ability to survive and proliferate in the intestinal tract. Genetic determinants of E. faecalis conferring these properties are largely unknown. Here we show that PrkC, a one-component signaling protein containing a eukaryotic-type Ser/Thr kinase domain, modulates inherent antimicrobial resistance and intestinal persistence of E. faecalis. An E. faecalis mutant lacking PrkC grows at a wild-type rate in the absence of antimicrobial stress but exhibits enhanced sensitivity to cell-envelope-active compounds, including antibiotics that target cell-wall biogenesis and bile detergents. Consistent with its bile sensitivity, the mutant was also impaired at persistence in the intestine of mice. Thus, PrkC regulates key physiological processes in E. faecalis associated with its success as a nosocomial pathogen. The predicted domain architecture of PrkC comprises a cytoplasmic kinase domain separated by a transmembrane segment from extracellular domains thought to bind uncross-linked peptidogly-can, suggesting that PrkC is a transmembrane receptor that monitors the integrity of the E. faecalis cell wall and mediates adaptive responses to maintain cell-wall integrity. Given its role in modulating traits of E. faecalis important for its ability to cause nosocomial infections, we suggest that the one-component signaling protein PrkC represents an attractive target for the development of novel therapies to prevent infections by antibiotic-resistant enterococci.
机译：抗生素耐药的肠球菌是医院获得性感染的主要原因。粪肠球菌作为重要的医院病原体的出现是由于其对某些抗生素的固有抗性以及其在肠道中生存和增殖的能力所致。粪肠球菌赋予这些特性的遗传决定因素在很大程度上是未知的。在这里，我们显示PrkC，一种包含真核生物型Ser / Thr激酶结构域的单组分信号蛋白，可调节粪肠球菌的固有抗药性和肠道持久性。缺乏PrkC的粪肠球菌突变体在没有抗微生物应力的情况下以野生型速率生长，但对细胞包膜活性化合物（包括靶向细胞壁生物发生的抗生素和胆汁去污剂）的敏感性增强。与其胆汁敏感性一致，该突变体在小鼠肠道中的持久性也受到损害。因此，PrkC调节粪肠球菌的关键生理过程，与其成功作为医院病原体有关。 PrkC的预测结构域结构包含一个胞质激酶结构域，该结构域由跨膜段与认为结合未交联的肽聚糖罐的胞外结构域隔开，这表明PrkC是一种跨膜受体，可监测粪肠球菌的细胞壁完整性并介导适应性维持细胞壁完整性的反应。鉴于其在调节粪肠球菌的性状中起着重要的作用，该特性对其引起医院内感染具有重要意义，因此我们认为，单组分信号蛋白PrkC代表着一种有吸引力的靶标，可用于开发新的疗法来预防由抗生素耐药性肠球菌引起的感染。

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