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Anthrax lethal toxin induces human endothelial cell apoptosis.

James E Kirby1

  • 1Department of Pathology, Division of Cancer Biology and Angiogenesis, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02215, USA. jekirby@bidmc.harvard.edu

Infection and Immunity
|December 23, 2003
PubMed
Summary

Bacillus anthracis lethal toxin directly harms human endothelial cells, causing apoptosis. This finding suggests a new target for anthrax therapies by understanding lethal toxin's vascular effects.

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Area of Science:

  • Microbiology
  • Pathogenesis
  • Toxicology

Background:

  • Bacillus anthracis is a dangerous biowarfare agent with high lethality.
  • Anthrax pathogenesis requires better understanding for effective therapies, especially for systemic disease.
  • While macrophages are implicated, direct damage to host vasculature is also suspected in anthrax.

Purpose of the Study:

  • To investigate the direct toxicity of Bacillus anthracis toxins on endothelial cells.
  • To determine if lethal toxin or edema toxin affects endothelial cell viability and apoptosis.
  • To explore the mechanisms by which anthrax toxins impact vascular cells.

Main Methods:

  • Cultured human microvascular and large vessel endothelial cells were exposed to lethal toxin and edema toxin.

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  • Endothelial cell viability was assessed, and apoptosis was measured using caspase assays.
  • Mitogen-activated protein kinase (MAPK) pathways (ERK, p38, JNK) in endothelial cells were analyzed following toxin exposure.

    • Main Results:

    • Lethal toxin, but not edema toxin, significantly reduced endothelial cell viability.
    • Lethal toxin induced caspase-dependent apoptosis in both microvascular and large vessel endothelial cells.
    • Lethal toxin inhibited phosphorylation of ERK, p38, and JNK pathways and induced cleavage of MAPK kinases.

    Conclusions:

    • Lethal toxin directly causes endothelial cell apoptosis, primarily through inhibition of the ERK pathway.
    • This endothelial cell toxicity likely contributes to vascular pathology and hemorrhage in systemic anthrax.
    • Targeting lethal toxin's effects on endothelial cells may offer novel therapeutic strategies for anthrax.