Figure 5.

Schematic representation of mechanism involved in M1 mediated restoration of mitochondrial function and anti-mycobacterial activity of THP-1 cells in the pre-disease model mimicking borderline risk cholesterol exposure. Prolonged exposure to sub-pathological levels of cholesterol leads to increase in intracellular lipid bodies, alteration in mitochondrial structure and function that support persistence of M.tb. Pharmacological intervention by M1 reversed changes in cholesterol treated infected macrophages, in terms of restoring structure and function of mitochondria and reducing intracellular lipid, thereby increasing the clearance of intracellular mycobacteria.