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

نویسندگان

  • A S Ibrahim
  • S G Filler
  • D Sanglard
  • J E Edwards
  • B Hube
چکیده

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.

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Candida albicans secreted aspartyl proteinases in virulence and pathogenesis.

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عنوان ژورنال:
  • Infection and immunity

دوره 66 6  شماره 

صفحات  -

تاریخ انتشار 1998