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皮拉克洛斯特罗宾通过定数感应诱导大肠杆菌的多抗生素耐药性:一个新的视角
Kaikai Qin1, Yirong Zhang1, Xiangyu Zhang1
1National Key Laboratory of Green Pesticide, College of Plant Protection, South China Agricultural University, Guangzhou 510642, China.
Journal of hazardous materials
|June 22, 2025
概括
杀菌剂pyraclostrobin在0.5mg/L时激活了细菌通信 (定数感应) 并导致大肠杆菌的基因突变,显著增加了抗生素耐药性. 谨慎使用杀菌剂对于减轻这种风险至关重要.
科学领域:
- 环境科学 环境科学
- 微生物学 微生物学
- 分子生物学分子生物学
背景情况:
- 抗生素耐药性对全球健康构成重大威胁.
- 非抗生素化学物质,如农药,可以加剧抗生素耐药性的发展.
- 定数感应 (QS) 是一种细菌通信系统,与抗生素耐药性有关.
研究的目的:
- 为了研究暴露于pyraclostrobin对Escherichia coli的定数感应 (QS) 和抗生素耐药性的影响.
- 阐明pyraclostrobin影响抗生素耐药性的分子机制.
主要方法:
- 埃舍里希亚大肠杆菌暴露于pyraclostrobin (0.5毫克/升).
- 对各种抗生素的最小抑制度 (MIC) 的评估.
- 对基因表达的分析,包括luxS,acrB,marA,ompC和ompF.
- 对QS抑制剂疗效的评估.
- 检测细胞膜损伤,氧化应激和基因突变.
主要成果:
- 皮拉克洛斯特罗宾激活了QS,在大肠杆菌中增加了抗生素耐药性的128倍.
- 皮拉克洛斯特罗宾上调了luxS基因表达,增加了AI-2水平并增强了QS.
- 这导致多药物排泄 (acrB, marA) 的表达增加,并减少了毛孔素 (ompC, ompF) 的表达.
- QS抑制恢复了对抗生素的敏感性.
- 皮拉克洛斯特罗宾诱导细胞膜损伤,氧化应激和基因突变,进一步促进耐药性.
结论:
- 暴露于pyraclostrobin刺激大肠杆菌的抗生素耐药性,通过激活QS和诱导基因突变.
- 这些发现强调了严格的杀菌剂应用的必要性,以制抗生素耐药性的发展.
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