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

被引：54
|
作者：
Ibrahim, AS
Filler, SG
Sanglard, D
Edwards, JE
Hube, B
机构：
[1] Univ Calif Los Angeles, Harbor Med Ctr, Div Infect Dis,Res & Educ Inst, St Johns Cardiovasc Res Ctr,Dept Med, Torrance, CA 90509 USA
[2] Univ Calif Los Angeles, Sch Med, Los Angeles, CA 90024 USA
[3] CHU Vaudois, Inst Microbiol, CH-1011 Lausanne, Switzerland
[4] Univ Hamburg, Inst Allgemeine Bot, AMP 3, D-22609 Hamburg, Germany
来源：
INFECTION AND IMMUNITY | 1998年 / 66卷 / 06期
关键词：
D O I：
10.1128/IAI.66.6.3003-3005.1998
中图分类号：
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号：
100102 ;
摘要：
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.
引用
收藏
页码：3003 / 3005
页数：3
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