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On-Chip Endothelial Inflammatory Phenotyping
Published on: July 22, 2012
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Alpha toxin from Clostridium perfringens induces proinflammatory changes in endothelial cells
M Bunting1, D E Lorant, A E Bryant
1The Eccles Program in Human Molecular Biology and Genetics, University of Utah, Salt Lake City, Utah 84112, USA.
The Journal of Clinical Investigation
|August 1, 1997
Summary
Clostridium perfringens alpha toxin triggers human endothelial cells to produce vasoactive lipids, platelet-activating factor (PAF) and prostacyclin, contributing to gas gangrene pathogenesis.
Area of Science:
- Microbiology
- Cell Biology
- Pathophysiology
Background:
- Alpha toxin from Clostridium perfringens type A is a phospholipase C implicated in gas gangrene.
- Endothelial cells play a crucial role in vascular homeostasis.
Purpose of the Study:
- To investigate the effects of alpha toxin on human endothelial cell synthesis of vasoactive lipids.
- To elucidate the mechanisms underlying alpha toxin-induced endothelial cell activation and neutrophil adhesion.
Main Methods:
- Treatment of cultured human endothelial cells with purified alpha toxin.
- Measurement of vasoactive lipid synthesis (PAF, prostacyclin).
- Assessment of neutrophil adhesion and P-selectin expression.
- In vivo studies using alpha toxin-injected rats.
Main Results:
- Alpha toxin stimulated endothelial cells to synthesize platelet-activating factor (PAF) and prostacyclin.
- PAF synthesis required the toxin's enzymatic activity and protein kinase C activation.
- Alpha toxin increased diacylglycerol and ceramide while decreasing phosphatidylcholine and sphingomyelin.
- Enhanced neutrophil adhesion to endothelial cells was mediated by the PAF receptor and P-selectin.
- P-selectin expression and neutrophil accumulation were observed in vivo.
Conclusions:
- Clostridium perfringens alpha toxin dysregulates endothelial cell function by inducing vasoactive lipid synthesis and promoting neutrophil adhesion.
- These toxin-mediated endothelial cell responses contribute to the pathogenesis of gas gangrene, including vascular permeability and inflammation.
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