Mycobacteria Infection and Lipid Droplets: Host and Pathogen Stealing, Sharing and Storing Fat

Mycobacterium tuberculosis is an acid-fast intracellular pathogen of macrophages and the etiological agent of the human respiratory disease tuberculosis (TB). A key aspect of the M. tuberculosis lifecycle is its ability to establish long-term persistent (i.e. latent) infection within the lungs of infected individuals. During latency, M. tuberculosis produces, stores, and utilizes lipid droplets containing the neutral fatty acid triacylglycerol. In many organisms including M. tuberculosis, lipid droplets have been shown to function as a long-term energy storage depots, providing energy for key metabolic pathways, and serving as a carbon source for the generation of important biosynthetic precursors. Failure of M. tuberculosis to generate, maintain, or utilize triacylglycerol stored within lipid droplets leads to reduced survival of the bacterium in in vitro and in vivo models of persistence. These findings implicate lipid droplets as central organelles vital to the physiology and pathogenesis of M. tuberculosis within the host. In this chapter, the persistence of M. tuberculosis in the context of lipid droplet biogenesis, storage, and utilization is discussed.