Curcumin enhances human macrophage control of Mycobacterium tuberculosis infection

Respirology. 2016 Jul;21(5):951-7. doi: 10.1111/resp.12762. Epub 2016 Mar 24.

Abstract

Background and objective: With the worldwide emergence of highly drug-resistant tuberculosis (TB), novel agents that have direct antimycobacterial effects or that enhance host immunity are urgently needed. Curcumin is a polyphenol responsible for the bright yellow-orange colour of turmeric, a spice derived from the root of the perennial herb Curcuma longa. Curcumin is a potent inducer of apoptosis-an effector mechanism used by macrophages to kill intracellular Mycobacterium tuberculosis (MTB).

Methods: An in vitro human macrophage infection model was used to determine the effects of curcumin on MTB survival.

Results: We found that curcumin enhanced the clearance of MTB in differentiated THP-1 human monocytes and in primary human alveolar macrophages. We also found that curcumin was an inducer of caspase-3-dependent apoptosis and autophagy. Curcumin mediated these anti-MTB cellular functions, in part, via inhibition of nuclear factor-kappa B (NFκB) activation.

Conclusion: Curcumin protects against MTB infection in human macrophages. The host-protective role of curcumin against MTB in macrophages needs confirmation in an animal model; if validated, the immunomodulatory anti-TB effects of curcumin would be less prone to drug resistance development.

Keywords: apoptosis; autophagy; curcumin; nuclear-factor kappa B; tuberculosis.

MeSH terms

  • Apoptosis* / drug effects
  • Apoptosis* / immunology
  • Curcumin / pharmacology*
  • Humans
  • Macrophages, Alveolar* / drug effects
  • Macrophages, Alveolar* / immunology
  • Models, Immunological
  • Mycobacterium tuberculosis / drug effects*
  • Mycobacterium tuberculosis / physiology
  • NF-kappa B / metabolism
  • Protective Agents / pharmacology
  • Tuberculosis* / immunology
  • Tuberculosis* / therapy

Substances

  • NF-kappa B
  • Protective Agents
  • Curcumin