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Related Experiment Videos

Oxidized ATP protection against anthrax lethal toxin.

Mahtab Moayeri1, Katherine E Wickliffe, Jason F Wiggins

  • 1Microbial Pathogenesis Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.

Infection and Immunity
|June 23, 2006
PubMed
Summary

Oxidized ATP (o-ATP) protects macrophages from Bacillus anthracis lethal toxin (LT) by preventing protective antigen (PA) oligomerization in endosomes. This finding offers a potential therapeutic strategy against anthrax toxin-induced cell death.

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Area of Science:

  • Cell Biology
  • Toxicology
  • Immunology

Background:

  • Bacillus anthracis lethal toxin (LT) causes rapid macrophage lysis, but the mechanism is unknown.
  • The ATP-activated P2X7 receptor is implicated in nucleotide-mediated macrophage lysis.
  • This study investigates the role of P2X7 receptors in LT-induced cytolysis.

Purpose of the Study:

  • To determine if P2X7 receptors mediate LT-induced macrophage lysis.
  • To identify the mechanism by which LT induces cell death.
  • To evaluate the therapeutic potential of P2X7 antagonists against anthrax toxin.

Main Methods:

  • Utilized P2X7 receptor antagonists, including oxidized ATP (o-ATP).
  • Assessed macrophage lysis, substrate cleavage, and PA oligomerization.

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  • Employed confocal microscopy with pH-sensitive dyes and in vivo mouse models.

    • Main Results:

    • Oxidized ATP (o-ATP) protected macrophages from LT-induced lysis.
    • o-ATP inhibited PA oligomerization within acidified endosomes but not at the cell surface.
    • o-ATP also protected against anthrax edema toxin and diphtheria toxin, increasing endosomal pH.
    • Mice treated with o-ATP and LT were protected from lethality.

    Conclusions:

    • P2X7 receptors and their antagonists play a role in LT-induced macrophage lysis.
    • LT-induced cell death is mediated by PA oligomerization in acidified endosomes.
    • o-ATP represents a potential therapeutic agent against anthrax toxin and other toxins requiring endosomal escape.