Bacterial persisters are phenotypic variants of an isogenic cell population that can survive antibiotic treatment and resume growth after the antibiotics have been removed. Cell dormancy has long been considered the principle mechanism underlying persister formation. However, dormancy alone is insufficient to explain the full range of bacterial persistence. Our recent work revealed that in addition to ‘passive defense’ via dormancy, persister cells employ ‘active defense’ via enhanced efflux activity to expel drugs. This finding suggests that persisters combine two seemingly contradictory mechanisms to tolerate antibiotic attack. Here, we review the passive and active aspects of persister formation, discuss new insights into the process, and propose new techniques that can facilitate the study of bacterial persistence.

细菌持久性是同基因细胞群的表型变异，可以在抗生素治疗后幸存并在去除抗生素后恢复生长。长期以来，细胞休眠一直被认为是持久性细胞形成的基本机制。但是，仅休眠是不足以解释细菌持久性的全部范围的。我们最近的工作表明，除通过休眠的“被动防御”外，持久性细胞还通过增强的外排活性来利用“主动防御”来驱逐药物。这一发现表明，坚持者结合了两种看似矛盾的机制来耐受抗生素的攻击。在这里，我们回顾了持久性物质形成的被动和积极方面，讨论了对该过程的新见解，并提出了可以促进细菌持久性研究的新技术。