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Visualization of Endoplasmic Reticulum Subdomains in Cultured Cells
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Perfringolysin O-Induced Plasma Membrane Pores Trigger Actomyosin Remodeling and Endoplasmic Reticulum Redistribution

Cláudia Brito1,2, Francisco S Mesquita1, Christopher K E Bleck3

  • 1i3S-Instituto de Investigação e Inovação em Saúde, IBMC, Universidade do Porto, 4099-002 Porto, Portugal.

Toxins
|July 20, 2019
PubMed

Insights

Clostridium perfringens perfringolysin O (PFO) disrupts cell membranes and reorganizes the cytoskeleton. This pore-forming toxin also damages the endoplasmic reticulum, impacting endothelial cells during infection.

Area of Science:

  • Microbiology
  • Cell Biology
  • Toxicology

Background:

  • Clostridium perfringens utilizes multiple toxins for severe infections.
  • Perfringolysin O (PFO) is a key pore-forming toxin contributing to C. perfringens pathogenesis.
  • The specific role of PFO in host cell damage remains incompletely understood.

Purpose of the Study:

  • To investigate the host cellular responses, particularly cytoskeletal changes, induced by purified PFO.
  • To elucidate the mechanisms underlying PFO-mediated plasma membrane and endoplasmic reticulum damage.

Main Methods:

  • Intoxication of human epithelial and endothelial cells with purified PFO.
  • Microscopic analysis of cytoskeletal reorganization and plasma membrane integrity.
  • Assessment of endoplasmic reticulum morphology and vacuolation.

Main Results:

  • Sub-lytic concentrations of PFO induced significant actomyosin cytoskeleton reorganization, forming cortical structures at sites of plasma membrane remodeling.
  • PFO-induced damage and recovery correlated with the assembly and disassembly of these cortical structures, requiring pore formation, calcium influx, and myosin II activity.
  • PFO disrupted the endoplasmic reticulum, leading to vacuolation, with ER-enriched vacuoles observed within cortical actomyosin structures.

Conclusions:

  • PFO, even at sub-lytic concentrations, profoundly affects host cell cytoskeleton and plasma membrane integrity.
  • The observed cellular events suggest PFO targets endothelial cell integrity early in C. perfringens infections.
  • PFO-induced disruption of the endoplasmic reticulum contributes to cellular damage.
Keywords:
actomyosin remodelingperfringolysin Oplasma membrane damagepore-forming toxins

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