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Enrichment and Detection of Clostridium perfringens Toxinotypes in Retail Food Samples
Published on: October 18, 2019
Cellular vacuolation induced by Clostridium perfringens epsilon-toxin
Masahiro Nagahama1, Yukari Itohayashi, Hideki Hara
1Department of Microbiology, Faculty of Pharmaceutical Sciences, Tokushima Bunri University, Tokushima, Japan. nagahama@ph.bunri-u.ac.jp
The FEBS Journal
|July 26, 2011
Summary
Clostridium perfringens epsilon-toxin oligomers form in cell membranes, are endocytosed, and induce cell vacuolation originating from late endosomes and lysosomes. This process is inhibited by specific agents and microtubule disruption.
Area of Science:
- Cell Biology
- Microbiology
- Toxicology
Background:
- Clostridium perfringens epsilon-toxin is a known cell-lethal agent.
- The toxin's mechanism of action, particularly vacuole formation, requires further elucidation.
Purpose of the Study:
- To investigate the mechanism by which epsilon-toxin induces vacuolation in Madin-Darby canine kidney cells.
- To determine the cellular pathway and origin of epsilon-toxin-induced vacuoles.
Main Methods:
- Dose- and time-dependent vacuolation assays.
- Confocal microscopy using specific cellular markers (e.g., EEA1, LAMP2, Rab5, Rab7).
- Inhibition studies using methyl-β-cyclodextrin, PEG 4000, bafilomycin A1, colchicine, and nocodazole.
Main Results:
- Epsilon-toxin induced vacuolation in a dose- and time-dependent manner.
- Toxin oligomers formed in lipid rafts were endocytosed and trafficked from early endosomes to late endosomes/lysosomes.
- Vacuole formation was dependent on late endosomal/lysosomal pathways and microtubule integrity, with Rab7 playing a crucial role.
Conclusions:
- Epsilon-toxin oligomers are endocytosed after formation in lipid rafts.
- The induced vacuoles originate from late endosomes and lysosomes, mediated by epsilon-toxin oligomers.
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