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Separation and Fractionation of Cell Wall and Cell Membrane Proteins from Mycobacterium tuberculosis for Downstream Protein Analysis
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A major role for ferroptosis in Mycobacterium tuberculosis-induced cell death and tissue necrosis

Eduardo P Amaral1, Diego L Costa2, Sivaranjani Namasivayam2

  • 1Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD eduardo.amaral@nih.gov.

The Journal of Experimental Medicine
|February 22, 2019
PubMed

Insights

Tuberculosis infection triggers ferroptosis, a cell death pathway involving iron and lipid damage. Inhibiting this pathway reduces bacterial load, suggesting a new therapeutic target for tuberculosis.

Area of Science:

  • Immunology
  • Cell Biology
  • Pathogen Biology

Background:

  • Necrotic cell death during Mycobacterium tuberculosis (Mtb) infection promotes pathogen spread.
  • Ferroptosis is a regulated necrosis driven by iron accumulation and lipid peroxidation.

Purpose of the Study:

  • To investigate the role of ferroptosis in Mtb-induced necrotic cell death.
  • To evaluate ferroptosis inhibition as a potential host-directed therapy for tuberculosis.

Main Methods:

  • Assessed Mtb-infected macrophage necrosis markers (glutathione, Gpx4, iron, lipid peroxidation).
  • Utilized ferroptosis inhibitor (Fer-1) and iron chelation in vitro and in vivo.
  • Quantified bacterial load in Fer-1 treated infected mice.

Main Results:

  • Mtb infection induced ferroptosis hallmarks in macrophages and mouse lungs.
  • Ferrostatin-1 and iron chelation suppressed Mtb-induced necrosis.
  • Ferrostatin-1 treatment significantly reduced bacterial burden in vivo.

Conclusions:

  • Ferroptosis is a key mechanism of necrosis in Mtb infection.
  • Targeting ferroptosis offers a promising host-directed therapeutic strategy for tuberculosis.

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