Boshoff Helena I M, Barry Clifton E
Tuberculosis Research Section, LIG/NIAID/NIH, Twinbrook II, Room 239, 12441 Parklawn Drive, Rockville, Maryland 20852, USA.
Nat Rev Microbiol. 2005 Jan;3(1):70-80. doi: 10.1038/nrmicro1065.
Human tuberculosis is a complex disease caused by bacterial populations that are located in discrete lesions (microenvironments) in a single host. Some of these microenvironments are conducive to replication, whereas others restrict bacterial growth without necessarily sterilizing the infecting microorganisms. The physical and biochemical milieu in these lesions is poorly defined. None of the existing animal models for tuberculosis (except perhaps non-human primates) reproduce the diversity of disease progression that is seen in humans. Nonetheless, transcriptomics and studies using bacterial mutants have led to testable hypotheses about metabolic functions that are essential for viability in the absence of replication. A complete picture of bacterial metabolism must balance reducing equivalents while maintaining an energized membrane and basic cellular processes.
人类结核病是一种复杂的疾病,由存在于单个宿主离散病灶(微环境)中的细菌群体引起。其中一些微环境有利于细菌繁殖,而另一些则会限制细菌生长,但不一定能杀灭感染微生物。这些病灶中的物理和生化环境尚不清楚。现有的结核病动物模型(可能非人类灵长类动物除外)均无法再现人类疾病进展的多样性。尽管如此,转录组学和使用细菌突变体的研究已经产生了关于代谢功能的可验证假设,这些功能在细菌不繁殖时对其生存至关重要。细菌代谢的完整图景必须在维持膜电位和基本细胞过程的同时平衡还原当量。