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Modification of epithelial cell barrier permeability and intercellular junctions by Clostridium sordellii lethal

Catherine Boehm1, Maryse Gibert, Blandine Geny

  • 1Unité des Bactéries anaérobies et Toxines, Institut Pasteur, 28 rue du Dr Roux, 75724, Paris Cedex 15, France.

Cellular Microbiology
|July 6, 2006
PubMed

Insights

Clostridium sordellii lethal toxins (LTs) alter epithelial barrier function by disrupting adherens junctions, not tight junctions. This occurs via Rac-dependent disorganization of basolateral actin filaments.

Area of Science:

  • Microbiology
  • Cell Biology
  • Toxicology

Background:

  • Clostridium sordellii lethal toxin (LT) is a glucosyltransferase.
  • LT inactivates small GTPases from the Rho and Ras families, crucial for cell signaling.
  • Epithelial barrier integrity is maintained by tight and adherens junctions, and the actin cytoskeleton.

Purpose of the Study:

  • To investigate the effects of two LT variants (LT82 and LT9048) on epithelial cell barrier integrity.
  • To elucidate the mechanisms by which LTs affect tight junctions, adherens junctions, and the actin cytoskeleton.
  • To determine the role of Rac GTPase in LT-induced barrier disruption.

Main Methods:

  • Using polarized Mouse Cortical Collecting Duct (MCCD) and Madin-Darby Canine Kidney (MDCK) cells.
  • Assessing the effects of LT82 and LT9048 on tight junction and adherens junction integrity.
  • Analyzing changes in the actin cytoskeleton and E-cadherin localization.
  • Investigating the involvement of Rac GTPase in the observed effects.

Main Results:

  • LTs showed limited effects on tight junctions.
  • LTs rapidly modified paracellular permeability (within 2-4 hours).
  • LTs induced basolateral actin filament disorganization but not apical actin changes.
  • LTs altered adherens junctions by causing E-cadherin-catenin complex removal from the membrane to the cytosol.
  • LT-induced adherens junction perturbation resulted from Rac-dependent disorganization of the basolateral actin cytoskeleton.

Conclusions:

  • Clostridium sordellii lethal toxins primarily disrupt epithelial barrier function by targeting adherens junctions.
  • The mechanism involves Rac-dependent disorganization of the basolateral actin cytoskeleton, essential for E-cadherin function.
  • These findings highlight the dynamic equilibrium of actin filaments in maintaining epithelial barrier integrity.

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