PPARγ Expression and Function in Mycobacterial Infection: Roles in Lipid Metabolism, Immunity, and Bacterial Killing

Figure 1

Model of PPARγ functions in mycobacterial infection. The activation of macrophage TLR2 signaling by M. tuberculosis, ManLAM, or M. bovis BCG results in the activation of PPARγ and NF-κB. The activation of PPARγ by mycobacterial infection induces lipid droplet formation, PGE₂ production and favors mycobacterial survival. Moreover, the PPARγ activation can down-modulate NF-κB activity inhibiting the proinflammatory cytokine production. Both inhibition of PPARγ with the selective antagonist GW9662 or PPARγ knockdown with siRNA result in a reduction of lipid droplet biogenesis and increased Mycobacterium killing by macrophages.