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Candida albicans  and  Candida glabrata  are predominant fungi associated with oral candidiasis. Histatin 5 (Hst 5) is a small cationic human salivary peptide with high fungicidal activity against  C. albicans , however many strains of  C. glabrata  are resistant. Since Hst 5 requires fungal binding to cell wall components prior to intracellular translocation, reduced Hst 5 binding to  C. glabrata  may be the reason for its insensitivity.  C. glabrata  has higher surface levels of β-1,3-glucans as compared with  C. albicans ; however these differences did not account for reduced Hst 5 uptake and killing in  C. glabrata . Similarly, the biofilm matrix of  C. glabrata  contained significantly higher levels of β-1,3-glucans compared with  C. albicans , but it did not reduce the percentage of Hst 5 positive fungal cells in the biofilm. Hst 5 enters  C. albicans  cell through polyamine transporters Dur3p and Dur31p that are uncharacterized in  C. glabrata .  C. glabrata  strains expressing Ca Dur3  and Ca Dur31  had two-fold higher killing and uptake of Hst 5. Thus, neither  C. glabrata  cell surface or biofilm matrix β-1,3-glucan levels affected Hst 5 toxicity; rather the crucial rate limiting step is reduced uptake that can be overcome by expression of  C. albicans  Dur proteins in  C. glabrata .

Histatin 5 Resistance of Candida glabrata Can Be Reversed by Insertion of Candida albicans Polyamine Transporter-Encoding Genes DUR3 and DUR31