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Key tissue targets responsible for anthrax-toxin-induced lethality

Shihui Liu1, Yi Zhang, Mahtab Moayeri

  • 1Microbial Pathogenesis Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA. shliu@niaid.nih.gov

Nature
|September 3, 2013
PubMed

Insights

Bacillus anthracis toxins cause lethality by damaging distinct cell types. Anthrax lethal toxin (LT) targets heart and vascular cells, while oedema toxin (ET) primarily affects liver cells (hepatocytes).

Area of Science:

  • Microbiology
  • Toxicology
  • Pathophysiology

Background:

  • Bacillus anthracis causes anthrax via two exotoxins: lethal toxin (LT) and oedema toxin (ET).
  • The specific host cell targets responsible for the lethal effects of these toxins remain unidentified.
  • Capillary morphogenesis protein-2 (CMG2) is a known receptor for these toxins.

Purpose of the Study:

  • To elucidate the critical cell types targeted by anthrax lethal toxin (LT) and oedema toxin (ET) that lead to host mortality.
  • To investigate the role of the anthrax toxin receptor CMG2 in mediating toxin-induced lethality across different cell types.

Main Methods:

  • Generation of cell-type-specific CMG2-null and CMG2-expressing mice.
  • Challenging these genetically modified mice with purified anthrax lethal toxin (LT) and oedema toxin (ET).
  • Assessing the contribution of specific cell types to toxin-induced mortality.

Main Results:

  • Lethality from LT involves damage to cardiomyocytes and vascular smooth muscle cells.
  • ET-induced lethality is primarily mediated through its action on hepatocytes.
  • Contrary to previous hypotheses, endothelial cell targeting by LT or ET does not significantly contribute to mortality.

Conclusions:

  • Bacillus anthracis employs LT and ET to induce host lethality by coordinately damaging distinct vital organ systems.
  • LT and ET exhibit differential cell-type tropism, targeting separate critical cellular populations for lethal effects.
  • Endothelial cells are not a primary target for anthrax toxin-induced lethality.

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