Secreted aspartyl proteinases and interactions of Candida albicans with human endothelial cells

Abstract

The endothelial cell interactions of homozygous null mutants of Candida albicans that were deficient in secreted aspartyl proteinase 1 (Sap1), Sap2, or Sap3 were investigated. Only Sap2 was found to contribute to the ability of C. albicans to damage endothelial cells and stimulate them to express E- selectin. None of the Saps studied appears to play a role in C. albicans adherence to endothelial cells.