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Peroxisomal ROS control cytosolic Mycobacterium tuberculosis replication in human macrophages

Enrica Pellegrino1, Beren Aylan1, Claudio Bussi1

  • 1Host-pathogen interactions in Tuberculosis Laboratory, The Francis Crick Institute, London, UK.

The Journal of Cell Biology
|September 22, 2023
PubMed

Insights

Human macrophages increase peroxisomes to combat Mycobacterium tuberculosis (Mtb). These organelles generate reactive oxygen species (ROS) to eliminate cytosolic Mtb, revealing a novel antimicrobial defense mechanism.

Area of Science:

  • Cell Biology
  • Immunology
  • Microbiology

Background:

  • Peroxisomes are vital organelles involved in metabolism and immune responses.
  • The role of peroxisomes in eliminating bacteria within macrophages is not fully understood.
  • Mycobacterium tuberculosis (Mtb) infection presents a significant challenge to host immunity.

Purpose of the Study:

  • To investigate the function of peroxisomes in human macrophages during Mtb infection.
  • To elucidate the mechanisms by which peroxisomes contribute to bacterial control.
  • To determine the role of the ESX-1 secretion system in Mtb-induced peroxisome biogenesis.

Main Methods:

  • Utilized induced pluripotent stem cell-derived human macrophages (iPSDM).
  • Infected iPSDM with wild-type Mtb and an ESX-1 deficient mutant.
  • Employed genetically encoded localization-dependent ROS probes to measure ROS production.

Main Results:

  • Mtb infection triggers peroxisome biogenesis, dependent on the ESX-1 secretion system for cytosolic access.
  • Peroxisome-deficient macrophages allowed Mtb replication, indicating peroxisomes control cytosolic bacteria.
  • Peroxisomes were observed to increase reactive oxygen species (ROS) levels during Mtb infection.

Conclusions:

  • Human macrophages enhance peroxisome function to restrict Mtb infection.
  • Peroxisome-generated ROS are crucial for eliminating cytosolic Mtb.
  • This study reveals a novel peroxisome-mediated, ROS-dependent mechanism for controlling intracellular bacterial pathogens.

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