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Related Experiment Videos

Anthrax lethal toxin induces endothelial barrier dysfunction.

Jason M Warfel1, Amber D Steele, Felice D'Agnillo

  • 1Laboratory of Biochemistry and Vascular Biology, Division of Hematology, Center for Biologics Evaluation and Research, Food and Drug Administration, 29 Lincoln Drive, Bldg. 29, Rm. 129, Bethesda, MD 20892, USA.

The American Journal of Pathology
|May 28, 2005
PubMed
Summary
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Anthrax lethal toxin (LT) disrupts human lung endothelial cell barriers, increasing permeability. This dysfunction, involving actin and VE-cadherin changes, may contribute to systemic anthrax vascular damage.

Area of Science:

  • Cell Biology
  • Pathology
  • Toxicology

Background:

  • Systemic anthrax infection is characterized by hemorrhage and pleural effusion.
  • Anthrax lethal toxin (LT) is a key virulence factor of Bacillus anthracis.
  • Endothelial barrier function is crucial for vascular integrity.

Purpose of the Study:

  • To investigate the impact of anthrax lethal toxin (LT) on the barrier function of primary human lung microvascular endothelial cells.
  • To analyze the distribution of cytoskeletal actin and vascular endothelial-cadherin (VE-cadherin) under LT exposure.
  • To determine the role of LT-induced barrier dysfunction in systemic anthrax pathology.

Main Methods:

  • Primary human lung microvascular endothelial cells were cultured and treated with LT components (lethal factor [LF] and protective antigen [PA]).

Related Experiment Videos

  • Barrier function was assessed by measuring transendothelial electrical resistance and albumin permeability.
  • Cytoskeletal actin and VE-cadherin distribution were analyzed using immunofluorescence microscopy and cell surface enzyme-linked immunosorbent assay.

    • Main Results:

    • LT caused a concentration- and time-dependent decrease in barrier resistance and increased albumin permeability.
    • LT induced alterations in actin stress fibers and VE-cadherin distribution.
    • Neither LF, PA, nor a combination of inactive LF mutant and PA affected barrier function or protein distribution.
    • LT-induced barrier dysfunction was independent of endothelial apoptosis or necrosis.

    Conclusions:

    • Anthrax lethal toxin (LT) directly impairs human lung microvascular endothelial cell barrier function.
    • LT-induced changes in actin and VE-cadherin contribute to increased vascular permeability.
    • LT-mediated barrier dysfunction is a potential mechanism underlying vascular complications in systemic anthrax infection.