Changes in cellular metabolism have proven to be important factors in driving cell behavior. It has been shown that cellular metabolism of immune cells changes when exposed to or infected by several pathogens: while this is often an adaptation of the host cells to the infection, sometimes it represents a mechanism through which the pathogens evade immune activation. Borrelia burgdorferi sensu lato, the causative agent of Lyme borreliosis, is a pathogen that highly depends on the host to survive, as the bacterium lacks many central metabolic pathways to generate its own nutrients. It is therefore quite likely that the bacterium interacts with host cells to obtain these metabolites and thereby affects metabolism in the host. Previously, several studies have assessed metabolic pathways in B. burgdorferi s.l. and how it adapts to its different host species. However, few studies have looked into how the interaction with the bacterium might affect the host cell metabolism. In this review we present the major metabolic pathways activated during Lyme borreliosis, viewed from both bacterium and host metabolism, and we discuss how these pathways interact with each other, and how they influence pathogenesis of Lyme borreliosis.

已经证明细胞代谢的变化是驱动细胞行为的重要因素。已经表明，免疫细胞的细胞代谢在暴露于几种病原体或被几种病原体感染时会发生变化：尽管这通常是宿主细胞对感染的适应，但有时它代表了病原体规避免疫激活的机制。伯氏疏螺旋体（Berrelia burgdorferi sensu lato）是一种病原体，是一种高度依赖宿主生存的病原体，因为该细菌缺乏许多中央代谢途径来产生自身的营养。因此，细菌很可能与宿主细胞相互作用以获得这些代谢物，从而影响宿主的代谢。以前，有几项研究评估了新陈代谢中的代谢途径。B. burgdorferi sl及其如何适应其不同的寄主物种。但是，很少有研究探讨与细菌的相互作用如何影响宿主细胞的代谢。在这篇综述中，我们从细菌和宿主新陈代谢的角度介绍了莱姆氏疏液症激活期间激活的主要代谢途径，并讨论了这些途径如何相互影响，以及它们如何影响莱姆氏疏液症的发病机理。