Vitamin D3 induces autophagy in human monocytes/macrophages via cathelicidin

Cell Host Microbe. 2009 Sep 17;6(3):231-43. doi: 10.1016/j.chom.2009.08.004.


Autophagy and vitamin D3-mediated innate immunity have been shown to confer protection against infection with intracellular Mycobacterium tuberculosis. Here, we show that these two antimycobacterial defenses are physiologically linked via a regulatory function of human cathelicidin (hCAP-18/LL-37), a member of the cathelicidin family of antimicrobial proteins. We show that 1,25-dihydroxyvitamin D3 (1,25D3), the active form of vitamin D, induced autophagy in human monocytes via cathelicidin, which activated transcription of the autophagy-related genes Beclin-1 and Atg5. 1,25D3 also induced the colocalization of mycobacterial phagosomes with autophagosomes in human macrophages in a cathelicidin-dependent manner. Furthermore, the antimycobacterial activity in human macrophages mediated by physiological levels of 1,25D3 required autophagy and cathelicidin. These results indicate that human cathelicidin, a protein that has direct antimicrobial activity, also serves as a mediator of vitamin D3-induced autophagy.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antimicrobial Cationic Peptides / genetics
  • Antimicrobial Cationic Peptides / immunology*
  • Autophagy / drug effects*
  • Cathelicidins
  • Cells, Cultured
  • Cholecalciferol / pharmacology*
  • Host-Pathogen Interactions
  • Humans
  • Macrophages / cytology*
  • Macrophages / drug effects
  • Macrophages / microbiology
  • Monocytes / cytology*
  • Monocytes / drug effects
  • Monocytes / microbiology
  • Mycobacterium tuberculosis / physiology
  • Tuberculosis / genetics
  • Tuberculosis / immunology
  • Tuberculosis / microbiology
  • Tuberculosis / physiopathology*


  • Antimicrobial Cationic Peptides
  • Cholecalciferol
  • Cathelicidins