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Death pathways activated in CaCo-2 cells by Clostridium perfringens enterotoxin
Ganes Chakrabarti1, Xin Zhou, Bruce A McClane
1Department of Molecular Genetics and Biochemistry, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15261, USA.
Infection and Immunity
|July 23, 2003
Summary
Clostridium perfringens enterotoxin (CPE) triggers distinct cell death pathways. Lower doses induce apoptosis via caspase 3/7, while higher doses cause oncosis, both relevant to gastrointestinal disease.
Area of Science:
- Cell Biology
- Microbiology
- Toxicology
Background:
- Clostridium perfringens enterotoxin (CPE) is a key virulence factor.
- CPE causes cytotoxic effects in intestinal cells.
Purpose of the Study:
- To elucidate the mammalian cell death pathways activated by CPE.
- To differentiate the mechanisms of CPE-induced cell death at varying concentrations.
Main Methods:
- CaCo-2 cell cultures were treated with different doses of CPE.
- Inhibitors of oncosis (glycine) and caspases were utilized.
- Morphological damage and DNA cleavage were assessed.
Main Results:
- Lower CPE doses induced caspase 3/7-dependent apoptosis, involving mitochondrial pathways.
- Higher CPE doses triggered oncosis, confirmed by glycine's inhibitory effect.
- Both cell death pathways were dose-dependent.
Conclusions:
- CPE elicits distinct cell death mechanisms, apoptosis and oncosis, based on concentration.
- These findings have implications for understanding CPE-associated gastrointestinal diseases.
- Both apoptosis and oncosis may contribute to intestinal pathology during CPE infection.