Department of Pathobiology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.
Department of Pathobiology, Division of Food Microbiology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.
Curr Pharm Biotechnol. 2023;24(15):1898-1915. doi: 10.2174/1389201024666230411110002.
Relapse infection usually results from resistance to the antibiotic, acquired genes, or persister cells. Persister cells are formed through mutation, reduced activity or metabolically inactive pathways induced by antibiotics, harassing conditions, low ATP, and malnutrition. These factors provide the ground for bacteria to grow slowly. Such a slow growth rate makes traditional antibiotics ineffective against persister cells. , in addition to this form, can be observed in Small Colony Variants (SCVs), L-forms, and dormant, all of which are characterized by at least one feature, , slow growth. Despite their slow growth, they are metabolically active in terms of stringent SOS and cell wall stress responses. The stress response involves resistance against harassing conditions, and it survives until it is reactivated later. The present study aims to discuss the mechanisms of all persister cell formations, circumstances involved, gene mutation, and adoptable strategies against it.
复发感染通常是由于抗生素耐药性、获得的基因或休眠细胞引起的。休眠细胞是通过突变、抗生素诱导的活性降低或代谢不活跃途径、恶劣条件、低 ATP 和营养不良形成的。这些因素为细菌的缓慢生长提供了条件。这种缓慢的生长速度使得传统抗生素对休眠细胞无效。除了这种形式外,还可以在小菌落变种 (SCV)、L 型和休眠中观察到,所有这些都至少有一个特征,即生长缓慢。尽管它们的生长缓慢,但它们在严格的 SOS 和细胞壁应激反应方面具有代谢活性。应激反应涉及对恶劣条件的抵抗,并且它会存活下来,直到以后被重新激活。本研究旨在讨论所有休眠细胞形成的机制、涉及的情况、基因突变以及针对休眠细胞的可采用策略。