Adherence of Candida albicans to endothelial cells is inhibited by prostaglandin I2.

The adherence of Candida species yeast cells to bovine and human endothelium was measured. The adherence phenomenon is a saturable event which can be altered by the release of prostaglandin I2 (PGI2 or prostacyclin) by endothelial cells. Release of PGI2 by endothelium has a protective effect, reducing Candida albicans yeast cell adherence to endothelial cells in a dose-dependent manner. Conversely, C. albicans appears to inhibit the release of PGI2 by endothelial cells and thus perhaps is capable of increasing the number of yeast cells which adhere to endothelium. Furthermore, a long-acting analog of PGI2, carbacyclin, reduced the number of yeast cells adhering to human platelet aggregates. Thus, it is possible that the release of PGI2 by endothelium has a protective effect against the hematogenous dissemination of C. albicans and its ability to adhere to vascular endothelium and fibrin-platelet matrices.