Abstract

Adherence of Candida albicans yeast cells to mammalian cells in vitro is promoted by a cell-surface adhesin that is probably a mannan or a mannoprotein. This observation is based on results of studies that utilized either lectins or antibodies to Candida that block attachment. Selective enzymatic degradation of cell wall constituents has been used to define the surface ligand of the candidal cell. Recently, nonadhering, spontaneous mutants of C. albicans, from both yeast and mycelial forms, that lack specific mannoproteins have been described. In addition, such mutants are avirulent, an indication that attachment plays a role in the disease process. The mammalian receptor for Candida has not been identified, but in endocarditis it could be fibronectin, both because fibronectin is present at the endocardial lesion and because those Candida species that bind to fibronectin in vitro exhibit a high disease potential; i.e., Candida species that bind to fibronectin in vitro also cause endocarditis, while those that do not bind in vitro do not cause disease. Attachment of yeast cells both to human buccal and vaginal epithelial cells is reduced significantly if yeast cells are preincubated with fibronectin, a finding that indicates a possible role for fibronectin as the epithelial surface receptor for Candida.

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