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Infect Immun, June 1998, p. 3003-3005, Vol. 66, No. 6
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

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

Ashraf S. Ibrahim,1,* Scott G. Filler,1,2 Dominique Sanglard,3 John E. Edwards Jr.,1,2 and Bernhard Hube4

Division of Infectious Diseases, St. John's Cardiovascular Research Center, Department of Medicine, Harbor-UCLA Research and Education Institute, Torrance, California 905091; UCLA School of Medicine, Los Angeles, California 900242; Institut de Microbiologie, Centre Hospitalier Universitaire Vaudois, CH 1011 Lausanne, Switzerland3; and Institut für Allgemeine Botanik, AMP III, Universität Hamburg, D-22609 Hamburg, Germany4

Received 30 October 1997/Returned for modification 25 November 1997/Accepted 26 March 1998

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.

* Corresponding author. Mailing address: Division of Infectious Diseases, St. John's Cardiovascular Research Center, Harbor-UCLA Medical Center, Bldg. R-B2, 1000 West Carson St., Torrance, CA 90509. Phone: (310) 222-3813. Fax: (310) 782-2016. E-mail: Ibrahim{at}AFP76.HUMC.EDU.

Infect Immun, June 1998, p. 3003-3005, Vol. 66, No. 6
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


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