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A striking and clinically relevant virulence trait of the human fungal pathogen  Candida albicans  is its ability to grow and switch reversibly among different morphological forms. Inhibition of yeast-to-hypha transition in  C .  albicans  represents a new paradigm for antifungal intervention. We have previously demonstrated the novel antifungal activity of purpurin against  Candida  fungi. In this study, we extended our investigation by examining the  in   vitro  effect of purpurin on  C .  albicans  morphogenesis and biofilms. The susceptibility of  C .  albicans  biofilms to purpurin was examined quantitatively by 2,3-bis(2-methoxy-4-nitro-5-sulfo-phenyl)-2H-tetrazolium-5-carboxanilide reduction assay. Hyphal formation and biofilm ultrastructure were examined qualitatively by scanning electron microscopy (SEM). Quantitative reverse transcription-PCR (qRT-PCR) was used to evaluate the expression of hypha-specific genes and hyphal regulator in purpurin-treated fungal cells. The results showed that, at sub-lethal concentration (3 µg/ml), purpurin blocked the yeast-to-hypha transition under hypha-inducing conditions. Purpurin also inhibited  C .  albicans  biofilm formation and reduced the metabolic activity of mature biofilms in a concentration-dependent manner. SEM images showed that purpurin-treated  C .  albicans  biofilms were scanty and exclusively consisted of aggregates of blastospores. qRT-PCR analyses indicated that purpurin downregulated the expression of hypha-specific genes ( ALS3 ,  ECE1 ,  HWP1 ,  HYR1 ) and the hyphal regulator  RAS1 . The data strongly suggested that purpurin suppressed  C .  albicans  morphogenesis and caused distorted biofilm formation. By virtue of the ability to block these two virulence traits in  C .  albicans , purpurin may represent a potential candidate that deserves further investigations in the development of antifungal strategies against this notorious human fungal pathogen  in   vivo .

Purpurin Suppresses Candida albicans Biofilm Formation and Hyphal Development