Mycobacterium tuberculosis exploits human interferon γ to stimulate macrophage extracellular trap formation and necrosis

Ka Wing Wong, Williams R. Jacobs

Research output: Contribution to journalArticle

52 Scopus citations


Human neutrophils form extracellular traps during M. tuberculosis infection, but a similar phenomenon has not been reported in human macrophages. Here we demonstrate that M. tuberculosis induces release of extracellular traps from human macrophages. This process is regulated by elastase activity, previously shown to regulate formation of extracellular traps by neutrophils. Interestingly, formation of extracellular traps by macrophages during M. tuberculosis infection is inducible by interferon γ (IFN-γ). These traps are mainly produced by heavily infected macrophages. Accordingly, IFN-γ is found to stimulate M. tuberculosis aggregation in macrophages. Both IFN-γ-inducible events, extracellular trap formation and mycobacterial aggregation, require the ESX-1 secretion system. In addition, IFN-γ is found to enhance ESX-1-mediated macrophage necrosis. In the absence of ESX-1, IFN-γ does not restore any extracellular trap formation, mycobacterial aggregation, or macrophage necrosis. Thus, initial characterization of macrophage extracellular trap formation due to M. tuberculosis infection led to the uncovering of a novel role for IFN-γ in amplifying multiple effects of the mycobacterial ESX-1.

Original languageEnglish (US)
Pages (from-to)109-119
Number of pages11
JournalJournal of Infectious Diseases
Issue number1
StatePublished - Jul 1 2013



  • ESX-1
  • M. tuberculosis
  • extracellular traps
  • human macrophages
  • interferon-γ
  • necrosis

ASJC Scopus subject areas

  • Immunology and Allergy
  • Infectious Diseases

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