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Simvastatin decreases the silver resistance of E. faecalis through compromising the entrapping function of extracellular polymeric substances against silver
World Journal of Microbiology and Biotechnology ( IF 4.0 ) Pub Date : 2020-03-14 , DOI: 10.1007/s11274-020-02830-5
Jingwen Cui 1 , Mengting Duan 1 , Qing Sun 1 , Wei Fan 1
Affiliation  

Enterococcus faecalis (E. faecalis) is a Gram-positive bacterium closely related to many refractory infections of human and shows the resistant ability against the antibacterial effects of silver. Simvastatin is a semisynthetic compound derived from lovastatin and a hydroxymethyl glutaryl coenzyme A(HMG-COA) reductase inhibitor showing certain inhibitive effects on bacteria. The main purpose of this study was to establish and characterize the Ag+/silver nanoparticles (AgNPs)-resistant E. faecalis, and further evaluate the function of extracellular polymeric substances (EPS) in the silver resistance and the effect of simvastatin on the silver-resistance of E. faecalis. The results showed that the established silver-resistant E. faecalis had strong resistance against both Ag+ and AgNPs and simvastatin could decrease the silver-resistance of both original and Ag+/AgNPs-resistant E. faecalis. The Transmission electron microscopy (TEM), High-angle annular dark-field (HAADF) and mapping images showed that the silver ions or particles aggregated and confined in the EPS on surface areas of the cell membrane when the silver-resistant E. faecalis were incubated with Ag+ or AgNPs. When the simvastatin was added, the silver element was not confined in the EPS and entered the bacteria. These findings may indicate that the silver resistance of E. faecalis was derived from the entrapping function of EPS, but simvastatin could compromise the function of EPS to decrease the silver resistant ability of E. faecalis.

中文翻译:

辛伐他汀通过破坏细胞外聚合物对银的捕获功能来降低粪肠球菌的银抗性

粪肠球菌(E. faecalis)是一种革兰氏阳性菌,与人类多种难治性感染密切相关,对银的抗菌作用具有抗药性。辛伐他汀是一种衍生自洛伐他汀和羟甲基戊二酰辅酶 A(HMG-COA) 还原酶抑制剂的半合成化合物,对细菌显示出一定的抑制作用。本研究的主要目的是建立和表征抗 Ag+/银纳米粒子 (AgNPs) 的粪肠球菌,并进一步评估胞外聚合物 (EPS) 在抗银中的作用以及辛伐他汀对银-粪肠球菌的抗性。结果表明,已建立的耐银 E. 粪肠球菌对 Ag+ 和 AgNPs 都有很强的抗性,辛伐他汀可以降低原始和抗 Ag+/AgNPs 的粪肠球菌的银抗性。透射电子显微镜 (TEM)、高角度环形暗场 (HAADF) 和映射图像显示,当耐银粪肠球菌处于细胞膜表面区域时,银离子或颗粒聚集并限制在细胞膜表面区域的 EPS 中。与 Ag+ 或 AgNPs 孵育。加入辛伐他汀后,银元素没有被限制在EPS中,而是进入了细菌中。这些发现可能表明粪肠球菌的银抗性来源于EPS的包埋功能,但辛伐他汀可能会损害EPS的功能从而降低粪肠球菌的抗银能力。透射电子显微镜 (TEM)、高角环形暗场 (HAADF) 和映射图像显示,当耐银粪肠球菌处于细胞膜表面时,银离子或颗粒聚集并限制在细胞膜表面区域的 EPS 中。与 Ag+ 或 AgNPs 孵育。加入辛伐他汀后,银元素没有被限制在EPS中,而是进入了细菌中。这些发现可能表明粪肠球菌的银抗性来源于EPS的包埋功能,但辛伐他汀可能会损害EPS的功能从而降低粪肠球菌的抗银能力。透射电子显微镜 (TEM)、高角度环形暗场 (HAADF) 和映射图像显示,当耐银粪肠球菌处于细胞膜表面区域时,银离子或颗粒聚集并限制在细胞膜表面区域的 EPS 中。与 Ag+ 或 AgNPs 孵育。加入辛伐他汀后,银元素没有被限制在EPS中,而是进入了细菌中。这些发现可能表明粪肠球菌的银抗性来源于EPS的包埋功能,但辛伐他汀可能会损害EPS的功能从而降低粪肠球菌的抗银能力。粪便与 Ag+ 或 AgNPs 一起孵育。加入辛伐他汀后,银元素没有被限制在EPS中,而是进入了细菌中。这些发现可能表明粪肠球菌的银抗性来源于EPS的包埋功能,但辛伐他汀可能会损害EPS的功能从而降低粪肠球菌的抗银能力。粪便与 Ag+ 或 AgNPs 一起孵育。加入辛伐他汀后,银元素没有被限制在EPS中,而是进入了细菌中。这些发现可能表明粪肠球菌的银抗性来源于EPS的包埋功能,但辛伐他汀可能会损害EPS的功能从而降低粪肠球菌的抗银能力。
更新日期:2020-03-14
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