Abstract
BackgroundThe 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.MethodsThe 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 conclusionsMagnolol 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 SignificanceThis study provides useful information towards the development of new strategies to reduce the incidence of C. albicans biofilm-associated infection.
Highlights
Candida albicans is one of the most common pathogens, and is associated with the occurrence of mortality rates as high as 35–50% [1,2]
Magnolol and honokiol inhibited adhesion, the transition from yeast to hypha, and biofilm formation by C. albicans through the Ras1-cyclic AMP-dependent Protein (cAMP)-Efg1 pathway
Magnolol and honokiol exhibited antifungal activity in the in vivo C. elegans assay system In C. elegans, we found that infection with C. albicans SC5314 induced a significant (P < 0.0001) decrease in lifespan of the nematodes compared with control (Fig. 9A)
Summary
Candida albicans is one of the most common pathogens, and is associated with the occurrence of mortality rates as high as 35–50% [1,2]. Infection by C. albicans involves adhesion to host cells or implanted medical devices as the first step, and this is followed by hyphal growth and biofilm formation [3,4,5,6,7]. The pathogenicity of C. albicans is closely related to its ability to change between two morphological forms, yeast and hyphae [7,8] This transition is highly regulated and involves multiple interconnected signaling pathways, including the cyclic AMP-dependent Protein (cAMP) Kinase A and the Cph1-mediated Mitogen-Activated Protein Kinase (MAPK) [7]. 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. Development of new antifungals with inhibitory action on adhesion, yeast-hyphal transition and biofilm formation by C. albicans is very necessary
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
