Borrelia burgdorferi hijacks cellular metabolism of immune cells: Consequences for host defense.

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.