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Clostridium perfringens Delta-Toxin Induces Rapid Cell Necrosis

Soshi Seike1, Kazuaki Miyamoto1, Keiko Kobayashi1

  • 1Department of Microbiology, Faculty of Pharmaceutical Sciences, Tokushima Bunri University, Yamashiro-cho, Tokushima 770-8514, Japan.

Plos One
|January 26, 2016
PubMed

Insights

Clostridium perfringens delta-toxin induces cell death via necrosis. This pore-forming toxin damages cell membranes, leading to ATP depletion and mitochondrial dysfunction, independent of apoptosis.

Area of Science:

  • Microbiology
  • Cell Biology
  • Toxicology

Background:

  • Clostridium perfringens delta-toxin is a beta-pore-forming toxin implicated in C. perfringens types B and C pathogenicity.
  • The precise mechanism underlying delta-toxin's cytotoxicity remains largely unelucidated.

Purpose of the Study:

  • To investigate the cell death mechanisms induced by Clostridium perfringens delta-toxin.
  • To determine the role of lipid rafts and mitochondrial damage in delta-toxin-mediated cytotoxicity.

Main Methods:

  • Exposure of five distinct cell lines (A549, A431, MDCK, Vero, Caco-2) to delta-toxin.
  • Assessment of cytotoxicity, ATP levels, lipid raft integrity, mitochondrial membrane potential, and apoptosis markers (annexin V, propidium iodide, caspase-3, DNA fragmentation).
  • Liposome-based assays to evaluate toxin interaction with cholesterol-rich membranes.

Main Results:

  • Delta-toxin induced rapid cell swelling and ATP depletion across all tested cell lines.
  • Toxin oligomerization and binding occurred primarily in plasma membrane lipid rafts, and their disruption inhibited toxicity.
  • Evidence of mitochondrial membrane permeability damage and cytochrome c release was observed, alongside an increase in necrotic cells (annexin V-negative, propidium iodide-positive).
  • No DNA fragmentation or caspase-3 activation was detected, ruling out apoptosis.

Conclusions:

  • Clostridium perfringens delta-toxin mediates cell death through necrosis.
  • The toxin's mechanism involves targeting lipid rafts, causing mitochondrial damage, and ultimately leading to non-apoptotic cell death.

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