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首页> 外文期刊>Antimicrobial agents and chemotherapy. >Extracellular DNA impedes the transport of vancomycin in Staphylococcus epidermidis biofilms preexposed to subinhibitory concentrations of vancomycin
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Extracellular DNA impedes the transport of vancomycin in Staphylococcus epidermidis biofilms preexposed to subinhibitory concentrations of vancomycin

机译：细胞外DNA阻止万古霉素在表皮葡萄球菌生物膜中的运输，该生物膜预先受到亚抑制浓度的万古霉素

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摘要

Staphylococcus epidermidis biofilm formation is responsible for the persistence of orthopedic implant infections. Previous studies have shown that exposure of S. epidermidis biofilms to sub-MICs of antibiotics induced an increased level of biofilm persistence. BODIPY FL-vancomycin (a fluorescent vancomycin conjugate) and confocal microscopy were used to show that the penetration of vancomycin through sub-MIC-vancomycin-treated S. epidermidis biofilms was impeded compared to that of control, untreated biofilms. Further experiments showed an increase in the extracellular DNA (eDNA) concentration in biofilms preexposed to sub-MIC vancomycin, suggesting a potential role for eDNA in the hindrance of vancomycin activity. Exogenously added, S. epidermidis DNA increased the planktonic vancomycin MIC and protected biofilm cells from lethal vancomycin concentrations. Finally, isothermal titration calorimetry (ITC) revealed that the binding constant of DNA and vancomycin was 100- fold higher than the previously reported binding constant of vancomycin and its intended cellular D-Ala-D-Ala peptide target. This study provides an explanation of the eDNA-based mechanism of antibiotic tolerance in sub-MIC-vancomycin-treated S. epidermidis biofilms, which might be an important factor for the persistence of biofilm infections.
机译：表皮葡萄球菌生物膜的形成负责整形外科植入物感染的持续存在。先前的研究表明，表皮葡萄球菌生物膜暴露于抗生素的亚MICs会导致生物膜持久性水平提高。 BODIPY FL-万古霉素（荧光万古霉素偶联物）和共聚焦显微镜检查显示，与未处理的对照生物膜相比，经万古霉素处理的表皮葡萄球菌生物膜的渗透受到阻碍。进一步的实验表明，预先暴露于亚MIC万古霉素的生物膜中细胞外DNA（eDNA）浓度增加，表明eDNA在阻碍万古霉素活性方面的潜在作用。外源添加表皮葡萄球菌DNA可增加浮游万古霉素MIC，并保护生物膜细胞免受致命万古霉素浓度的影响。最后，等温滴定热法（ITC）显示，DNA和万古霉素的结合常数比先前报道的万古霉素及其预期的细胞D-Ala-D-Ala肽靶标的结合常数高100倍。这项研究提供了一种基于eDNA的在MIC-万古霉素治疗的表皮葡萄球菌生物膜中抗生素耐药性的机制的解释，这可能是生物膜感染持续存在的重要因素。

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