Curcumin enhances human macrophage control of Mycobacterium tuberculosis infection

Background and objectiveWith 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 apoptosisan effector mechanism used by macrophages to kill intracellular Mycobacterium tuberculosis (MTB). MethodsAn in vitro human macrophage infection model was used to determine the effects of curcumin on MTB survival. ResultsWe 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 (NFB) activation. ConclusionCurcumin 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. The effects of curcumin (a polyphenol of tumeric) on Mycobacterium tuberculosis (MTB) infection using human macrophages were investigated in this study. Curcumin reduced the intracellular burden of MTB in infected macrophages through inhibition of NFB activation resulting in the induction of caspase-3-dependent apoptosis and autophagy.