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PPAR Research
Volume 2012 (2012), Article ID 383829, 7 pages
Review Article

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

1Laboratório de Imunofarmacologia, Instituto Oswaldo Cruz, Fundação Oswaldo Cruz, 21045-900 Rio de Janeiro, RJ, Brazil
2Laboratório de Biologia Celular, Departamento de Biologia, Universidade Federal de Juiz de Fora, 36036-900 Juiz de Fora, MG, Brazil

Received 14 January 2012; Revised 30 March 2012; Accepted 18 May 2012

Academic Editor: Jesse Roman

Copyright © 2012 Patricia E. Almeida et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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 ) activation by mycobacteria is not fully understood, recent findings are beginning to uncover a critical role for PPAR during mycobacterial infection. Here, we will review the molecular mechanisms that regulate PPAR expression and function during mycobacterial infection. Current evidence indicates that mycobacterial infection causes a time-dependent increase in PPAR expression through mechanisms that involve pattern recognition receptor activation. Mycobacterial triggered increased PPAR expression and activation lead to increased lipid droplet formation and downmodulation of macrophage response, suggesting that PPAR expression might aid the mycobacteria in circumventing the host response acting as an escape mechanism. Indeed, inhibition of PPAR enhances mycobacterial killing capacity of macrophages, suggesting a role of PPAR in favoring the establishment of chronic infection. Collectively, PPAR is emerging as a regulator of tuberculosis pathogenesis and an attractive target for the development of adjunctive tuberculosis therapies.