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

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PPAR Research
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Disciplines
  • Medicine

Abstract

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.

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