对耐卡巴胺复合物Enterobacter cloacae携带mcr-9的单独分离物中诱导的对聚米辛的耐药性的转录组分析
Jiming Wu1, Longjin Liu1, Jianmin Wang1
1Department of Microbiology, Yongchuan Hospital of Chongqing Medical University, Chongqing, China.
Journal of global antimicrobial resistance
|May 16, 2024
概括
耐卡巴胺复合体Enterobacter cloacae复合体 (CRECC) 中的多素耐药性因mcr-9基因表达而恶化. 高mcr-9表达和PhoPQ系统对于CRECC中的多素耐药性至关重要.
科学领域:
- 微生物学 微生物学
- 遗传学 是一个遗传学.
- 生物化学 生物化学
背景情况:
- 聚米克辛是对抗多药耐药格拉姆阴性细菌的关键的最后手段抗生素.
- 通过等离子体介导的移动多素抗性基因 (mcr) 的出现对多素的有效性构成重大威胁,特别是在耐卡巴胺的Enterobacter cloacae复合体 (CRECC) 中.
研究的目的:
- 阐明聚米辛诱导的细菌耐药性背后的机制.
- 调查mcr-9基因过度表达对CRECC中的多素耐药性的影响.
主要方法:
- 一种携带mcr-9基因的临床CRECC菌株 (CRECC414) 接受了聚胺治疗.
- 最低抑制度 (MIC) 用微稀释来确定.
- 基因表达水平,包括mcr-9,通过RT-qPCR进行评估.
- 全基因组测序 (WGS) 和转录组测序被用来识别与耐药性相关的遗传和转录组变异.
- 在基因组层面进行了代谢网络分析.
主要成果:
- 聚米辛治疗导致mcr-9表达的增加和MIC的显著升高.
- WGS和转录基因数据显示了arnBCADTEF基因盒子的大量上调,表明Arn/PhoPQ系统介导的L-Ara4N修饰是关键的抵抗机制.
- 在多药物排泄,氧化应激和修复途径,细胞膜生物合成和碳水化合物代谢中观察到基因表达的显著变化.
结论:
- 聚胺治疗严重破坏了细菌细胞的重要通路.
- 功能性的PhoPQ双组件系统对于Enterobacter cloacae的多素耐药性是不可或缺的,无论mcr-9表达率高.
- 这些发现为CRECC中的多素耐药机制提供了关键的见解,指导了未来的研究和治疗策略.
关键词:
抗微生物耐药性 抗微生物耐药性抗卡巴烯的 Enterobacter cloacae 复合体具有抗卡巴烯的作用.波利米克辛 (Polymyxin) 是一种多重的药物.文字转录学 (Transcriptomics) 是一个学科.mcr-9-9的使用情况.更多相关视频
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