**5.1. Scavenger receptor mediated lipid droplet biogenesis in** *M. tuberculosis*

Upon infection with pathogenic bacteria macrophages generate reactive oxygen species (ROS). The release of ROS generates oxidative stress, and results not only in damage to cellular structures but also to oxidation of fatty acids, such as low density lipoproteins (OxLDL) in granulomas. The binding of OxLDL to type 1 scavenger receptors CD36 and LOX1 induces increased surface expression of both receptors, leading to uptake of OxLDL [96-98]. In addition, CD36 increases the uptake of *M. tuberculosis* by macrophages [99]. The increased rate of OxLDL uptake results in the accumulation of oxidized lipids, which finally leads to the formation of foamy macrophages [98]. *M. tuberculosis* and *M. leprae* benefit from the accumulated OxLDL in the infected macrophage. OxLDL-laden lung macrophages show enhanced replication of intracellular *M. tuberculosis* compared to macrophages loaded with non-oxidized LDL [98]. The presence of oxidized phospholipids in *M. leprae* infected macrophages down-regulates the innate immune response and contributes to pathogenesis [92]. Moreover, scavenger receptordeficient phagocytes are characterized by a reduced intracellular bacterial survival and a lower cytokine response [100].
