Reduction in Pathogenicity in Yeast-like Fungi by Farnesol in Quail Model

Simple Summary Despite the discoveries of new therapeutic antimycotics, the development of drug resistance is still the main clinical challenge in the treatment of mycoses. Data on the presence of new phytopreparations, along with the direct fungicidal effects that interfere with the resistance of fungal pathogens located in the biofilm, are of great interest. The use of these compounds as monotherapies or in combination with known antimycotics may be an effective strategy for preventing and/or destroying Candida biofilms found on the surface of biomedical devices and in vivo. The action mechanisms of farnesol in fungi have yet to be fully understood, but they are complex and likely include several mechanisms such as growth inhibition and apoptosis promotion. Candida albicans was the first eukaryotic microorganism to exhibit quorum-sensing through the secretion of the sesquiterpene E, farnesol. This molecule is generated by dephosphorylation of farnesyl pyrophosphate in the mevalonate biosynthetic pathway in mammalian and yeast cells. Exogenous farnesol inhibits yeast-to-hyphal formation in a concentration- and time-dependent manner at the earliest stage of hyphal development. Much research has been devoted to studying the role of farnesol as an inhibitor of hyphal morphogenesis; however, little research has been published regarding the in vivo impacts of farnesol on fungal virulence and the development of Candida infection. While other studies have examined the impact of multiple doses of farnesol in addition to antimycotics, we hypothesize that C. albicans treated with a single dose of this quorum-sensing molecule could reduce fungal virulence in a quail model.