Affordable Access

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

PPAR Research
Publication Date
  • Medicine


Tuberculosis continues to be a global health threat, with drug resistance and HIV coinfection presenting challenges for its control. Mycobacterium tuberculosis, the etiological agent of tuberculosis, is a highly adapted pathogen that has evolved different strategies to subvert the immune and metabolic responses of host cells. Although the significance of peroxisome proliferator-activated receptor gamma (PPAR 𝛾 ) activation by mycobacteria is not fully understood, recent findings are beginning to uncover a critical role for PPAR 𝛾 during mycobacterial infection. Here, we will review the molecular mechanisms that regulate PPAR 𝛾 expression and function during mycobacterial infection. Current evidence indicates that mycobacterial infection causes a time-dependent increase in PPAR 𝛾 expression through mechanisms that involve pattern recognition receptor activation. Mycobacterial triggered increased PPAR 𝛾 expression and activation lead to increased lipid droplet formation and downmodulation of macrophage response, suggesting that PPAR 𝛾 expression might aid the mycobacteria in circumventing the host response acting as an escape mechanism. Indeed, inhibition of PPAR 𝛾 enhances mycobacterial killing capacity of macrophages, suggesting a role of PPAR 𝛾 in favoring the establishment of chronic infection. Collectively, PPAR 𝛾 is emerging as a regulator of tuberculosis pathogenesis and an attractive target for the development of adjunctive tuberculosis therapies.

There are no comments yet on this publication. Be the first to share your thoughts.


Seen <100 times