在Mycobacterium tuberculosis中逆转抗生素耐药性
Nicolas Blondiaux1, Martin Moune1, Matthieu Desroses2,3
1Univ. Lille, CNRS, Inserm, CHU Lille, Institut Pasteur de Lille, U1019-UMR8204-CIIL-Center for Infection and Immunity of Lille, F-59000 Lille, France.
Science (New York, N.Y.)
|March 18, 2017
概括
研究人员开发了一种新型分子SMARt-420,用于对抗结核病的抗生素耐药性. 这种小分子 (SMARt-420) 重新激活了休眠途径,克服了对乙胺的耐药性,并清除了小鼠的感染.
科学领域:
- 微生物学
- 药物发现
- 抗菌药物耐药性
背景情况:
- 抗生素耐药性,特别是多药耐药性和广泛耐药性结核菌,构成了全球严重的健康威胁.
- 许多关键的抗结核抗生素是前期药物,耐药性通常来自它们的细菌生物活化途径的突变.
研究的目的:
- 开发新型类似药物的分子,
- 确定可以克服*Mycobacterium结核病*现有的抗药机制的化合物.
主要方法:
- 针对替代生物激活途径的小分子的设计和合成.
- 对候选分子进行体外和体内检测,以检测耐埃西奥纳米德菌株 (Mycobacterium tuberculosis).
- 评估SMARt-420在清除感染和调节细菌敏感性的有效性.
主要成果:
- 开发了一种新型分子SMARt-420 (小分子流产抵抗),用于激活埃西奥纳米德的神秘生物激活途径.
- 在* Mycobacterium tuberculosis*中,SMARt-420显示出完全逆转埃西奥纳米德获得的耐药性的能力.
- 在小鼠模型中,用SMARt-420治疗成功清除了耐乙胺的感染,并增加了细菌对乙胺的敏感性.
结论:
- SMARt-420代表了一流的治疗策略,用于对抗结核病的埃西奥纳米德耐药性.
- 针对替代生物活化途径提供了一种有希望的方法来克服抗菌素耐药性.
- 这种策略有可能恢复现有的抗生素对抗耐药细菌菌株的疗效.
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