Wayne L G, Sohaskey C D
Department of Veterans Affairs Medical Center, Tuberculosis Research Laboratory (151), Long Beach, California 90822, USA.
Annu Rev Microbiol. 2001;55:139-63. doi: 10.1146/annurev.micro.55.1.139.
There is ample clinical evidence, as well as evidence from animal experiments, that Mycobacterium tuberculosis can persist in tissues for months to decades without replicating, yet with the ability to resume growth and activate disease. Our knowledge of both macrophage physiology and the nature of tuberculous lesions in man and animals suggests that hypoxia is a major factor in inducing nonreplicating persistence (NRP) of tubercle bacilli. In vitro models reinforce this conclusion and provide insights into mechanisms that make NRP possible. There is evidence from in vitro models that the strategies employed by the bacilli to permit hypoxic NRP include restriction of biosynthetic activity to conserve energy, induction of alternative energy pathways, and stabilization of essential cell components to lessen the need for repair or replacement.
有充分的临床证据以及动物实验证据表明,结核分枝杆菌可在组织中持续存在数月至数十年而不进行复制,但仍具备恢复生长并引发疾病的能力。我们对巨噬细胞生理学以及人类和动物结核病变本质的了解表明,缺氧是诱导结核杆菌非复制性持续存在(NRP)的主要因素。体外模型强化了这一结论,并为使NRP成为可能的机制提供了深入见解。体外模型的证据表明,杆菌用于实现缺氧NRP的策略包括限制生物合成活动以保存能量、诱导替代能量途径以及稳定基本细胞成分以减少修复或替换的需求。