Cutting edge: Vitamin D regulates lipid metabolism in Mycobacterium tuberculosis infection

J Immunol. 2014 Jul 1;193(1):30-34. doi: 10.4049/jimmunol.1400736. Epub 2014 Jun 4.


Vitamin D has long been linked to resistance to tuberculosis, an infectious respiratory disease that is increasingly hard to treat because of multidrug resistance. Previous work established that vitamin D induces macrophage antimicrobial functions against Mycobacterium tuberculosis. In this article, we report a novel, metabolic role for vitamin D in tuberculosis identified through integrated transcriptome and mechanistic studies. Transcriptome analysis revealed an association between vitamin D receptor (VDR) and lipid metabolism in human tuberculosis and infected macrophages. Vitamin D treatment of infected macrophages abrogated infection-induced accumulation of lipid droplets, which are required for intracellular M. tuberculosis growth. Additional transcriptomics results showed that vitamin D downregulates the proadipogenic peroxisome proliferator-activated receptor γ (PPARγ) in infected macrophages. PPARγ agonists reversed the antiadipogenic and the antimicrobial effects of VDR, indicating a link between VDR and PPARγ signaling in regulating both vitamin D functions. These findings suggest the potential for host-based, adjunct antituberculosis therapy targeting lipid metabolism.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Line, Tumor
  • Humans
  • Lipid Metabolism / drug effects*
  • Lipid Metabolism / immunology
  • Mycobacterium tuberculosis / immunology*
  • PPAR gamma / immunology
  • Receptors, Calcitriol / immunology
  • Transcriptome / drug effects*
  • Transcriptome / immunology
  • Tuberculosis / drug therapy
  • Tuberculosis / immunology*
  • Tuberculosis / pathology
  • Vitamin D / pharmacology*
  • Vitamins / pharmacology*


  • PPAR gamma
  • Receptors, Calcitriol
  • VDR protein, human
  • Vitamins
  • Vitamin D