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首页> 外文期刊>International journal of antimicrobial agents >Upregulation of icaA, atlE and aap genes by linezolid but not vancomycin in Staphylococcus epidermidis RP62A biofilms
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Upregulation of icaA, atlE and aap genes by linezolid but not vancomycin in Staphylococcus epidermidis RP62A biofilms

机译:利奈唑胺而非万古霉素在表皮葡萄球菌RP62A生物膜中上调icaA,atlE和aap基因

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Biofilms are complex bacterial structures protected by a self-produced polymer matrix that enables survival in hostile environments. Biofilms are more resistant to antibiotics than their planktonic counterparts and are therefore more difficult to eradicate. The aim of this study was to investigate the influence of vancomycin and linezolid on the maintenance of staphylococcal biofilms and their effect on the expression of biofilm-associated genes in Staphylococcus epidermidis. Pre-formed biofilms of S. epidermidis RP62A were challenged with linezolid and vancomycin at different concentrations as well as at their clinically relevant target concentration (15 mg/L) over time. Expression of icaA, atlE, aap, rnalll, luxS, sarA, rsbU and icaR genes following 2 h of exposure to these antibiotics was determined by quantitative PCR. Vancomycin did not significantly affect the biofilm under the tested conditions. However, linezolid affected the biofilm structure at concentrations of >2 mg/L (P<0.05); moreover, the exposure time to this antibiotic was a determinant for biofilm eradication. The level of transcription of icaA, aap and atlE increased by 5.18-, 2.58- and 3.06-fold, respectively, in biofilms exposed to linezolid, but no changes were observed for vancomycin. The other genes were not affected by these antibiotics. This study demonstrated that linezolid was effective in eradicating biofilms formed by S. epidermidis RP62A. Under the conditions tested, linezolid upregulated biofilm-associated genes probably due to the stress caused by low-dose antibiotic stimulation. In this study, linezolid showed better performance than vancomycin against staphylococcal biofilms.
机译:生物膜是受自我产生的聚合物基质保护的复杂细菌结构,能够在恶劣的环境中生存。生物膜比浮游生物膜对抗生素的抵抗力更高,因此更难根除。这项研究的目的是调查万古霉素和利奈唑胺对葡萄球菌生物膜的维持及其对表皮葡萄球菌生物膜相关基因表达的影响。随着时间的推移,预先用不同浓度的利奈唑胺和万古霉素挑战表皮葡萄球菌RP62A的生物膜,并使其达到临床相关的目标浓度(15 mg / L)。通过定量PCR确定暴露于这些抗生素2小时后icaA,atlE,aap,rnalll,luxS,sarA,rsbU和icaR基因的表达。万古霉素在测试条件下没有显着影响生物膜。然而,利奈唑胺在> 2 mg / L的浓度下会影响生物膜结构(P <0.05);此外,这种抗生素的暴露时间是根除生物膜的决定性因素。在暴露于利奈唑胺的生物膜中,icaA,aap和atlE的转录水平分别增加了5.18-,2.58-和3.06倍,但万古霉素未见变化。其他基因不受这些抗生素的影响。这项研究表明,利奈唑胺在根除表皮葡萄球菌RP62A形成的生物膜方面有效。在测试条件下,利奈唑胺上调了生物膜相关基因,可能是由于低剂量抗生素刺激引起的压力。在这项研究中,利奈唑胺在抗葡萄球菌生物膜方面显示出比万古霉素更好的性能。

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