Dwyer Daniel J, Kohanski Michael A, Collins James J
Howard Hughes Medical Institute, Department of Biomedical Engineering, Center for BioDynamics and Center for Advanced Biotechnology, Boston University, 44 Cummington Street, Boston, MA 02215, USA.
Curr Opin Microbiol. 2009 Oct;12(5):482-9. doi: 10.1016/j.mib.2009.06.018. Epub 2009 Jul 31.
The alarming spread of bacterial strains exhibiting resistance to current antibiotic therapies necessitates that we elucidate the specific genetic and biochemical responses underlying drug-mediated cell killing, so as to increase the efficacy of available treatments and develop new antibacterials. Recent research aimed at identifying such cellular contributions has revealed that antibiotics induce changes in metabolism that promote the formation of reactive oxygen species, which play a role in cell death. Here we discuss the relationship between drug-induced oxidative stress, the SOS response and their potential combined contribution to resistance development. Additionally, we describe ways in which these responses are being taken advantage to combat bacterial infections and arrest the rise of resistant strains.
对当前抗生素疗法呈现耐药性的细菌菌株惊人地扩散,这就需要我们阐明药物介导的细胞杀伤背后的特定遗传和生化反应,以提高现有治疗方法的疗效并开发新型抗菌药物。最近旨在确定此类细胞作用的研究表明,抗生素会诱导新陈代谢发生变化,从而促进活性氧的形成,而活性氧在细胞死亡中发挥作用。在此,我们讨论药物诱导的氧化应激、SOS反应之间的关系,以及它们对耐药性发展的潜在综合作用。此外,我们还描述了利用这些反应来对抗细菌感染并阻止耐药菌株增加的方法。