The aim of this study was to investigate the antibiofilm activity of coumarin against Candida albicans.

The efficacy of coumarin against biofilm formation and the mature biofilm of C. albicans was quantified by crystal violet (CV) staining and the 2,3-bis (2-methoxy-4-nitro-5-sulfophenyl)-5-[(phenylamino)carbonyl]-2H-tetrazolium hydroxide (XTT) reduction assay. The effect of coumarin on C. albicans adhesion was assessed on polystyrene plates and by using the cell surface hydrophobicity (CSH) assay. The morphological transition of C. albicans was conducted in two types of hyphae-inducing media at 37°C. The expression of hypha/biofilm-related genes was evaluated using qRT-PCR analysis. A rescue experiment involving addition of exogenous cyclic adenosine monophosphate (cAMP) was performed to investigate the involvement of cAMP in the yeast-to-hyphae transition. A C. albicans-infected Caenorhabditis elegans model was used to test the anti-virulence efficacy of coumarin.

Treatment with coumarin strongly affected the capacity of C. albicans to form biofilm and significantly impaired the preformed mature biofilm. The addition of coumarin notably inhibited C. albicans adhesion, CSH, and filamentation. The expression of some adhesion- and hypha-related genes, including HWP1, HYR1, ECE1, and ALS3, was remarkably down-regulated upon exposure to coumarin. Supplementation with cAMP partly rescued the coumarin-induced defects in hyphal development. Finally, coumarin prolonged survival in C. albicans-infected nematodes.

Coumarin inhibited C. albicans biofilm, which was associated with attenuated adhesion and hyphal growth.