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Autophagy in Mycobacterium tuberculosis infection: a passepartout to flush the intruder out?

Delia Goletti1, Elisa Petruccioli, Alessandra Romagnoli

  • 1Translational Research Unit, Department of Epidemiology and Preclinical Research, INMI, Rome, Italy.

Cytokine & Growth Factor Reviews
|February 12, 2013
PubMed

Insights

Mycobacterium tuberculosis evades autophagy, a key immune process, and exploits it for survival. Autophagy also plays a role in drug efficacy against tuberculosis.

Area of Science:

  • Cellular Biology
  • Immunology
  • Microbiology

Background:

  • Tuberculosis (TB), caused by Mycobacterium tuberculosis (M. tuberculosis), is a significant global health issue.
  • M. tuberculosis establishes latent infections by evading host immune responses.
  • Autophagy is a crucial cellular degradation pathway involved in immunity against intracellular pathogens.

Purpose of the Study:

  • To review the molecular strategies M. tuberculosis uses to subvert autophagy.
  • To explore how M. tuberculosis manipulates autophagy for its own benefit.
  • To discuss autophagy's multifaceted roles in anti-TB immunity and drug action.

Main Methods:

  • Literature review focusing on molecular mechanisms of M. tuberculosis-autophagy interaction.
  • Analysis of studies on autophagy's role in innate and adaptive immunity to tuberculosis.
  • Examination of research on autophagy's impact on the efficacy of anti-TB drugs.

Main Results:

  • M. tuberculosis employs specific mechanisms to resist autophagic clearance.
  • The bacterium hijacks the autophagy pathway to enhance its survival and persistence.
  • Autophagy contributes to immune responses against M. tuberculosis and potentiates drug activity.

Conclusions:

  • Understanding M. tuberculosis's manipulation of autophagy is key to combating latent infections.
  • Autophagy represents a potential therapeutic target for tuberculosis treatment.
  • Further research into autophagy's role can lead to novel strategies for TB drug development.
Keywords:
Anti-tuberculosis drugsAutophagyAutophagy gene polymorphismsInflammatory cytokinesMycobacterium tuberculosis

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