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Type I IFN-mediated NET release promotes Mycobacterium tuberculosis replication and is associated with granuloma

Chanchal Sur Chowdhury1, Rachel L Kinsella1, Michael E McNehlan1

  • 1Department of Molecular Microbiology, Center for Women's Infectious Disease Research, Washington University School of Medicine, St. Louis, MO 63110, USA.

Cell Host & Microbe
|December 5, 2024
PubMed

Insights

Neutrophil extracellular traps (NETs) promote Mycobacterium tuberculosis (Mtb) replication by releasing citrullinated histones. Type I interferon facilitates NET release, offering a potential target to inhibit Mtb pathogenesis.

Area of Science:

  • Immunology
  • Microbiology
  • Cell Biology

Background:

  • Neutrophils are abundant in tuberculosis airways.
  • Mycobacterium tuberculosis (Mtb) infection triggers neutrophil extracellular trap (NET) release.
  • The regulation and impact of NETs in Mtb pathogenesis are not well understood.

Purpose of the Study:

  • To investigate the molecular mechanisms regulating NET release during Mtb infection.
  • To determine the role of NETs in Mtb pathogenesis.
  • To identify potential therapeutic targets for tuberculosis.

Main Methods:

  • Studied histone citrullination by PAD4 in neutrophils during Mtb infection.
  • Investigated the role of type I interferon in NET formation and release.
  • Analyzed NETs in nonhuman primate granulomas.

Main Results:

  • PAD4-mediated histone citrullination enables NET release, maintaining neutrophil viability and promoting Mtb replication.
  • Type I interferon induces vesicle formation for NET release, preserving plasma membrane integrity.
  • NETs are associated with necrosis and caseation in nonhuman primate granulomas.

Conclusions:

  • NET release is a key mechanism in Mtb pathogenesis, regulated by PAD4 and type I interferon.
  • Targeting NET release presents a promising strategy for inhibiting Mtb.
  • Understanding NET regulation can lead to novel tuberculosis therapies.
Keywords:
PAD4bacterial pathogenesisgranulomahistone citrullinationmycobacteriumnecrosisneutrophil extracellular trapsneutrophilstuberculosistype I interferon

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