Abstract
Candida spp. are pathobionts, as they can switch from commensals to pathogens, responsible for a variety of pathological processes. Adhesion to surfaces, morphological switch and biofilm-forming ability are the recognized virulence factors promoting yeast virulence. Sessile lifestyle also favors fungal persistence and antifungal tolerance. In this study, we investigated, in vitro, the efficacy of two urinary cranberry metabolites, 5-(3′,4′-dihydroxy phenyl)-γ-valerolactone (VAL) and 4-hydroxybenzoic acid (4-HBA), in inhibiting C. albicans adhesion and biofilm formation. Both the reference strain SC5314 and clinical isolates were used. We evaluated biomass reduction, by confocal microscopy and crystal violet assay, and the possible mechanisms mediating their inhibitory effects. Both VAL and 4-HBA were able to interfere with the yeast adhesion, by modulating the expression of key genes, HWP1 and ALS3. A significant dose-dependent reduction in biofilm biomass and metabolic activity was also recorded. Our data showed that the two cranberry metabolites VAL and 4-HBA could pave the way for drug development, for targeting the very early phases of biofilm formation and for preventing genitourinary Candida infections.
Highlights
The Candida genus is the most common etiological agent of fungal opportunistic infections, ranging from superficial to mucosal and systemic diseases [1]
In a recent paper [11], we demonstrated that cranberry (Vaccinium macrocarpon) and its urinary metabolites are able to inhibit Candida biofilm formation in vitro, and we identified the most active compounds, which were recovered in the urines of subjects taking cranberry as a dietary supplement, responsible for the observed antifungal activity
We evaluated the expression of genes encoding for proteins that are involved in the initial phases of C. albicans biofilm formation
Summary
The Candida genus is the most common etiological agent of fungal opportunistic infections, ranging from superficial to mucosal and systemic diseases [1]. Infections often arise resulting from a derangement of equilibrium of the commensal yeast and the host [2]. Candida albicans is the most common species causing such infections, despite other Candida species being on the rise. C. albicans is a pleomorphic yeast that is able to filament and form biofilm on a variety of biotic and abiotic surfaces [3,4]. The biofilm architecture and the extracellular matrix released by fungal cells allow the fungus to persist within the host, resulting in recurrent infections. The biofilm-organized fungus displays an increased nonspecific tolerance to antifungal treatment, further impairing infection clearance [5]
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