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Related Experiment Videos

Anthrax toxin entry into polarized epithelial cells.

K E Beauregard1, S Wimer-Mackin, R J Collier

  • 1Departments of Microbiology, Harvard Medical School, Boston, Massachusetts, USA.

Infection and Immunity
|May 25, 1999
PubMed
Summary
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Anthrax edema toxin (EdTx) enters polarized T84 cells primarily through the basolateral surface, not the apical surface. This toxin entry mechanism differs from cholera toxin, highlighting distinct cellular pathways in disease causation.

Area of Science:

  • Cell Biology
  • Microbiology
  • Toxicology

Background:

  • Anthrax edema toxin (EdTx) is a binary toxin composed of anthrax edema factor (EF) and protective antigen (PA).
  • PA facilitates the delivery of EF into the cell cytosol, where it acts as an adenylate cyclase.
  • Understanding toxin entry mechanisms is crucial for developing targeted interventions.

Purpose of the Study:

  • To investigate the entry pathway of anthrax edema toxin (EdTx) into polarized human T84 epithelial cells.
  • To determine the role of cell surface polarity in EdTx cellular uptake.
  • To compare the entry mechanism of EdTx with that of cholera toxin (CT).

Main Methods:

  • Utilized polarized human T84 epithelial cells cultured on permeable supports.
  • Measured cyclic AMP-regulated chloride (Cl-) secretion as an indicator of toxin entry.

Related Experiment Videos

  • Assessed the binding of protective antigen (PA) to both apical and basolateral surfaces of T84 cells.
  • Investigated the association of the PA receptor with detergent-insoluble membranes.

    • Main Results:

    • EdTx induced significant Cl- secretion when applied to the basolateral surface, but not the apical surface.
    • Protective antigen (PA) binding was approximately 30-fold higher on the basolateral surface compared to the apical surface.
    • The PA receptor was found to be predominantly or exclusively located on the basolateral membrane.
    • PA receptor did not co-fractionate with caveola-like membranes, unlike cholera toxin receptors.

    Conclusions:

    • The basolateral membrane is the primary route for anthrax edema toxin entry into polarized T84 epithelial cells.
    • The cellular entry mechanism of EdTx is distinct from that of cholera toxin, involving different subcellular systems.
    • These findings provide insights into the specific nature of the PA receptor and its role in toxin pathogenesis.