Adding Another Piece to the Puzzle of Why NTM Infections Are Relatively Uncommon despite Their Ubiquitous Nature

Edward D Chan1,2,3,4, Adela Cota-Gomez4, Brendan Podell5

  • 1Rocky Mountain Regional Veterans Affairs Medical Center, Aurora, Colorado, USA ChanE@NJHealth.org.

Mbio
|April 21, 2021
PubMed

Insights

Nontuberculous mycobacteria (NTM) infections may stem from host susceptibility. Nuclear factor erythroid 2-related factor 2 (Nrf2) shows protective effects against NTM infection in mice, potentially via antioxidant pathways.

Area of Science:

  • Immunology
  • Microbiology
  • Genetics

Background:

  • Nontuberculous mycobacteria (NTM) are environmentally ubiquitous, yet NTM infections suggest underlying host susceptibility.
  • Classifying NTM disease into skin-soft tissue, lung, and disseminated forms aids in identifying unique host risk factors for each category.
  • Host susceptibility factors, both hereditary and acquired, are crucial for understanding the pathogenesis of NTM infections.

Purpose of the Study:

  • To explore the role of Nuclear factor erythroid 2-related factor 2 (Nrf2) in host defense against NTM infections.
  • To investigate potential mechanisms by which oxidative stress influences NTM susceptibility and Nrf2-mediated protection.
  • To build upon previous findings regarding Nrf2's protective role in a murine model of NTM infection.

Main Methods:

  • Utilized a murine model to study NTM infection.
  • Investigated the role of Nrf2, a transcription factor induced by oxidative stress.
  • Examined the effect of Nrf2 induction on Nramp-1 and phagosome-lysosome fusion.

Main Results:

  • Nrf2 was found to provide protection against NTM infection in a murine model.
  • Nrf2 induction of Nramp-1 was shown to enhance phagosome-lysosome fusion, a key antimicrobial mechanism.
  • The study suggests Nrf2 plays a significant role in the host's defense against NTM.

Conclusions:

  • Nrf2-mediated antioxidant responses are critical for host defense against NTM infections.
  • Oxidative stress may predispose individuals to NTM infections, while Nrf2 activation offers protection.
  • Further research into the interplay between oxidative stress, Nrf2, and NTM pathogenesis is warranted.

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