Department of Microbiology and Physiological Systems, University of Massachusetts Medical School, Worcester, Massachusetts 01655, USA.
Nat Rev Microbiol. 2016 Apr;14(4):221-34. doi: 10.1038/nrmicro.2016.12. Epub 2016 Mar 7.
Our understanding of bacterial pathogenesis is dominated by the cell biology of the host-pathogen interaction. However, the majority of metabolites that are used in prokaryotic and eukaryotic physiology and signalling are chemically similar or identical. Therefore, the metabolic crosstalk between pathogens and host cells may be as important as the interactions between bacterial effector proteins and their host targets. In this Review we focus on host-pathogen interactions at the metabolic level: chemical signalling events that enable pathogens to sense anatomical location and the local physiology of the host; microbial metabolic pathways that are dedicated to circumvent host immune mechanisms; and a few metabolites as central points of competition between the host and bacterial pathogens.
我们对细菌发病机制的理解主要基于宿主-病原体相互作用的细胞生物学。然而，大多数用于原核生物和真核生物生理和信号传导的代谢物在化学上是相似或相同的。因此，病原体和宿主细胞之间的代谢串扰可能与细菌效应蛋白与其宿主靶标之间的相互作用同样重要。在这篇综述中，我们重点讨论代谢水平上的宿主-病原体相互作用：使病原体能够感知宿主的解剖位置和局部生理学的化学信号事件；专门用于规避宿主免疫机制的微生物代谢途径；以及宿主和细菌病原体之间竞争的几个代谢物作为关键点。
