核糖体新生退出道中的非正规突变使Mycobacterium abscessus复合体产生克拉里思罗米辛耐药性
Wei Liao1, Xinyan Wang2, Yi Wang3
1Department of Pathogen Biology, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, China; High Altitude Health Science Research Centre of Tibet University, Medical College of Tibet University, Lhasa, China.
International journal of antimicrobial agents
|May 29, 2024
概括
在Mycobacterium abscessus中发现了克拉里素耐药性的新机制. 这些非正规的23S rRNA突变,在临床分离物中发现,可以改善对这种具有挑战性的感染的诊断.
科学领域:
- 微生物学 微生物学
- 遗传学 遗传学 是一个
- 分子生物学分子生物学
背景情况:
- 菌根杆菌疹导致全球肺部和皮肤感染.
- 在M. abscessus中克拉里素耐药性往往导致治疗失败.
- 正规的23S rRNA突变是已知的抵抗机制,但其他也存在.
研究的目的:
- 为了确定M. abscessus中克拉里素耐药性的新机制.
- 为了研究超出正规23SrRNA残留2270/2271.1.的突变.
主要方法:
- 从M. abscessus菌株中选择自发耐药突变物.
- 缺乏已知的抗性突变的突变体的全基因组测序.
- 临床分离物的局部定向突变发生和生物信息分析.
主要成果:
- 在23S rRNA (基转移酶中心,发针环) 中发现了非正规突变.
- 这些突变在临床M. abscessus隔离物中被发现.
- 引入的突变证实了对宏类耐药性的贡献,本地化在新生的类出口道附近.
结论:
- 几种非正规的23S rRNA突变在M. abscessus中赋予了清素耐药性.
- 这些发现扩大了对宏类药物耐药性的理解.
- 鉴定到的突变可以作为诊断标志物来检测克拉里菌素耐药性.
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