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Background  The first step in infection by  Candida albicans  is adhesion to host cells or implanted medical devices and this followed by hyphal growth and biofilm formation. Yeast-to-hyphal transition has long been identified as a key factor in fungal virulence. Following biofilm formation,  C .  albicans  is usually less sensitive or insensitive to antifungals. Therefore, development of new antifungals with inhibitory action on adhesion, yeast-hyphal transition and biofilm formation by  C .  albicans  is very necessary.    Methods  The effects of magnolol and honokiol on hypha growth were investigated using different induction media. Their inhibitory effects were determined using the 2,3-bis(2-methoxy-4-nitro-5-sulfophenyl)-2H-tetrazolium-5- carboxanilide assay, and biofilm thickness and viability were observed by a confocal scanning laser microscope. Mammalian cells were used in adhesion assays. Genes related to hyphae development and cell adhesions were analyzed by real-time reverse transcription-polymerase chain reaction. The exogenous cyclic adenosine monophosphate was used to determine the mechanisms of action of magnolol and honokiol.  Caenorhabditis elegans  was used as an  in vivo  model to estimate the antifungal activities of magnolol and honokiol.    Results and conclusions  Magnolol and honokiol inhibited adhesion, the transition from yeast to hypha, and biofilm formation by  C .  albicans  through the Ras1-cAMP-Efg1 pathway. Moreover, magnolol and honokiol prolonged the survival of nematodes infected by  C .  albicans . Magnolol and honokiol have potential inhibitory effects against biofilm formation by  C .  albicans .    General Significance  This study provides useful information towards the development of new strategies to reduce the incidence of  C .  albicans  biofilm-associated infection.

Effects of Magnolol and Honokiol on Adhesion, Yeast-Hyphal Transition, and Formation of Biofilm by Candida albicans