Mycobacterial Infection and Activation of Peroxisome Proliferator-Activated Receptors (PPARs): Role of Lipid Accumulation in Infected Cells

The present review discusses recent findings that describe the activation of peroxisome proliferator-activated receptors (PPARs) by mycobacterial infections and their role in determining the fate of bacilli by inducing lipid metabolism, anti-inflammatory function, and autophagy. The PPAR-
activation was mediated by the Middle East respiratory syndrome coronavirus (MERS-CoV)-derived S glycoprotein along with concurrent inhibition of macrophage responses and the suppression of proinflammatory cytokines. The cell wall of mycobacteria is made up of a lot of lipids with different molecular weights. To construct the cellular milieu necessary for their intracellular survival, some mycobacteria species hijack host cells and stimulate lipid droplet production. As a result, lipids are assumed to be critical for mycobacteria survival, invasion, parasitization, and multiplication within host cells. However, their physiological roles have not been fully elucidated. Mycobacteria modulate PPAR signaling and utilize host-derived triacyl-glycerol (TAG) and cholesterol as nutrient sources and for evasion of the host immune system. PPARs are important to the host-dependent mechanism of lipid metabolism and accumulation during mycobacterial infection.