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Examination of nanoparticle inactivation of Campylobacter jejuni biofilms using infrared and Raman spectroscopies.

机译:使用红外和拉曼光谱学检查空肠弯曲杆菌生物膜的纳米颗粒失活。

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Aims. To investigate inactivation effect and mechanism of zinc oxide nanoparticles (ZnO NPs) activity against Campylobacter jejuni biofilms. Methods and Results. ZnO NPs with concentrations of 0, 0.6, 1.2 and 6 mmol l--1 were employed in antimicrobial tests against Camp. jejuni planktonic cells and biofilms. Campylobacter jejuni sessile cells in biofilms were more resistant to a low concentration of ZnO NPs when compared to planktonic cells. The ZnO NPs penetrated the extracellular polymeric substance (EPS) without damage to the EPS and directly interacted with the sessile bacterial cells, as determined using infrared spectroscopy and scanning electron microscopy. Raman spectroscopy shows alterations in quinone structures and damage to nucleic acids following Camp. jejuni treatment with ZnO NPs. The mechanism of DNA damage is most likely due to the generation of reactive oxygen species (ROS). Spectroscopic-based partial least squares regression (PLSR) models could predict the number of surviving sessile cell numbers within a bacterial biofilm (>=log 4 CFU, root mean square error of estimation <0.36) from Fourier transform infrared (FT-IR) spectral measurements. Conclusions. ZnO NPs were found to have antimicrobial activity against Camp. jejuni biofilms. ZnO NPs penetrated the biofilm EPS within 1 h without damaging it and interacted directly with sessile cells in biofilms. Alterations in the DNA/RNA bases, which are owing to the generation of ROS, appear to result in Camp. jejuni cell death. Significance and Impact of the Study. ZnO NPs may offer a realistic strategy to eliminate Camp. jejuni biofilms in the environment.
机译:目的研究氧化锌纳米颗粒(ZnO NPs)对空肠弯曲杆菌生物膜的灭活作用及其机理。方法和结果。 ZnO NPs的浓度分别为0、0.6、1.2和6 mmol l -1 ,用于Camp的抗菌测试。空肠浮游细胞和生物膜。与浮游细胞相比,生物膜中的空肠弯曲杆菌无柄细胞对低浓度的ZnO NP更具抵抗力。 ZnO NPs渗透到细胞外聚合物质(EPS)中,而不会损坏EPS,并且直接与无柄细菌细胞发生相互作用,这是使用红外光谱和扫描电子显微镜确定的。拉曼光谱显示Camp后醌结构的改变和核酸的破坏。 ZnO NPs空肠治疗。 DNA损伤的机制最有可能是由于活性氧(ROS)的产生。基于光谱的偏最小二乘回归(PLSR)模型可以根据傅立叶变换红外(FT-IR)光谱预测细菌生物膜(> = log 4 CFU,估计均方根误差<0.36)中存活的无细胞数测量。结论。发现ZnO NPs对Camp具有抗菌活性。空肠生物膜。 ZnO NPs在1 h内穿透了生物膜EPS,而没有对其造成破坏,并直接与生物膜中的无柄细胞相互作用。 DNA / RNA碱基的改变(由于ROS的产生)似乎导致了Camp。空肠细胞死亡。研究的意义和影响。 ZnO NPs可能提供消除Camp的现实策略。空肠生物膜在环境中。

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