The main goal of the present work was to assess the effectiveness of zosteric acid (ZA) in hindering Escherichia coli biofilm formation on a mineral surface. Attenuated total reflectance-Fourier transform infrared (ATR-FTIR) flow system was used to probe in situ the biochemical changes induced by ZA on E. coli sessile cells growing on the zinc selenide ATR plate. Comparative proteome analysis was conducted on the sessile cells to better understand the principal molecular changes that occur on ZA-treated biofilms. The ZA treatment modified the kinetics of the biofilm development. After the ZA exposure, dramatic changes in the carbohydrates, proteins, and DNA profiles were observed over time in the ATR-FTIR spectra. These results were translated into the physiological effects such as the reduction of both the biomass and the EPS contents, the inhibition of the biofilm growth, and the promotion of the detachment. In E. coli sessile cells, the comparative proteome analysis revealed that, while the stress responses were upregulated, the pathways belonging to the DNA replication and repair were downregulated in the ZA-treated biofilms. The ZA reduced the binding capability of E. coli cells onto the ZnSe crystal, hindering the firm adhesion and the subsequent biofilm development on a mineral surface. The variation of the protein patterns indicated that the ZA acted as a stress factor on the sessile cells that seemed to discourage biomass proliferation, consequently decreasing the surface colonization.

中文翻译：

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矿物表面上经带环酸处理的大肠杆菌生物膜的生化和分子变化

当前工作的主要目标是评估带氢唑酸（ZA）阻止矿物表面上大肠杆菌生物膜形成的有效性。使用衰减的全反射傅里叶变换红外（ATR-FTIR）流动系统检测ZA诱导的硒化锌ATR平板上生长的大肠杆菌无柄细胞的生化变化。在无柄细胞上进行了比较蛋白质组分析，以更好地了解ZA处理的生物膜上发生的主要分子变化。ZA处理改变了生物膜发育的动力学。ZA暴露后，在ATR-FTIR光谱中观察到了碳水化合物，蛋白质和DNA随时间的急剧变化。这些结果转化为生理效应，例如减少生物量和EPS含量，抑制生物被膜的生长，促进分离。在大肠杆菌无柄细胞中，比较蛋白质组分析显示，虽然应激反应被上调，但在ZA处理的生物膜中属于DNA复制和修复的途径却被下调。ZA降低了大肠杆菌细胞与ZnSe晶体的结合能力，从而阻碍了牢固的粘附以及随后在矿物表面上形成生物膜。蛋白质模式的变化表明，ZA是无柄细胞上的应力因子，似乎抑制了生物量的增殖，因此减少了表面定殖。在ZA处理的生物膜中，属于DNA复制和修复的途径被下调。ZA降低了大肠杆菌细胞与ZnSe晶体的结合能力，从而阻碍了牢固的粘附以及随后在矿物表面上形成生物膜。蛋白质模式的变化表明，ZA是无柄细胞上的应力因子，似乎抑制了生物量的增殖，因此减少了表面定殖。在ZA处理的生物膜中，属于DNA复制和修复的途径被下调。ZA降低了大肠杆菌细胞与ZnSe晶体的结合能力，从而阻碍了牢固的粘附以及随后在矿物表面上形成生物膜。蛋白质模式的变化表明，ZA是无柄细胞上的应力因子，似乎抑制了生物量的增殖，因此减少了表面定殖。