Secreted Aspartyl Proteinases and Interactions of Candida albicans with Human Endothelial Cells

Author:

Ibrahim Ashraf S.1,Filler Scott G.12,Sanglard Dominique3,Edwards John E.12,Hube Bernhard4

Affiliation:

1. Division of Infectious Diseases, St. John’s Cardiovascular Research Center, Department of Medicine, Harbor-UCLA Research and Education Institute, Torrance, California 905091;

2. UCLA School of Medicine, Los Angeles, California 900242;

3. Institut de Microbiologie, Centre Hospitalier Universitaire Vaudois, CH 1011 Lausanne, Switzerland3; and

4. Institut für Allgemeine Botanik, AMP III, Universität Hamburg, D-22609 Hamburg, Germany4

Abstract

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.

Publisher

American Society for Microbiology

Subject

Infectious Diseases,Immunology,Microbiology,Parasitology

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