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Candida albicans stimulates endothelial cell eicosanoid production
S G Filler1, B O Ibe, P M Luckett
1Department of Internal Medicine, UCLA School of Medicine, Torrance 90509.
The Journal of Infectious Diseases
|November 11, 1991
Summary
Candida albicans invasion triggers endothelial cells to release prostaglandins, primarily prostaglandin I2 (PGI2). This response is linked to endothelial damage and phospholipase activity, impacting immune cell interactions.
Area of Science:
- Microbiology
- Immunology
- Cell Biology
Background:
- Human umbilical vein endothelial cells (HUVEc) play a role in inflammatory responses.
- Candida species are known opportunistic fungal pathogens.
- Endothelial cells produce eicosanoids, including prostaglandins, which modulate inflammation.
Purpose of the Study:
- To investigate the in vitro response of HUVEc to invasion by various Candida species.
- To determine the relationship between Candida-induced endothelial cell injury and eicosanoid release, specifically prostaglandin I2 (PGI2).
- To identify Candida species-specific factors contributing to endothelial cell activation and damage.
Main Methods:
- In vitro co-culture of HUVEc with different Candida species (e.g., C. albicans, C. glabrata, C. tropicalis).
- Measurement of eicosanoid release (prostaglandins) from endothelial cells.
- Assessment of endothelial cell injury.
- Detection of phospholipase activity in Candida species.
Main Results:
- Live Candida albicans significantly stimulated endothelial release of prostaglandins, predominantly PGI2.
- A strong correlation (r = .99) was observed between the capacity of Candida species to induce endothelial PGI2 release and their ability to cause endothelial injury.
- Only C. albicans exhibited phospholipase activity and was capable of stimulating PGI2 release and damaging endothelial cells.
- Candida glabrata and Candida tropicalis showed no phospholipase activity, nor did they induce significant PGI2 release or endothelial damage.
- Close proximity to germinated C. albicans was necessary for endothelial injury and PGI2 release.
Conclusions:
- Candida albicans-induced endothelial cell activation and injury are mediated by phospholipase activity.
- The release of PGI2 by endothelial cells in response to C. albicans may play a role in regulating neutrophil activity during fungal infections.
- Understanding these interactions is crucial for developing strategies against Candida-related endothelial complications.