is an opportunistic fungal pathogen that can cause systemic infections in immunocompromised individuals. Morphological transition and biofilm formation are major virulence factors of . Moreover, biofilm enhances resistance to antifungal agents. Therefore, it is urgent to identify new and effective compounds to target the biofilm of . In the present study, the antifungal activities of equol against were investigated. , the microdilution analysis and spot assay result showed that equol exhibited potent inhibitory activities against . Further investigations confirmed that the antifungal effects of equol involved interference with the transition from yeast to hypha and biofilm formation of . In addition, transcriptome sequencing and reverse transcription-quantitative PCR (qRT-PCR) analysis showed that equol significantly downregulated the expression of several genes in the Ras1-cAMP-PKA pathway related to hyphae and biofilm formation and significantly upregulated the expression of the negative transcriptional repressors and . Moreover, equol effectively reduced the production of cAMP, a key messenger in the Ras1-cAMP-PKA pathway, while supplementation with cAMP partly rescued the equol-induced defects in hyphal development. Furthermore, in a mouse model of systemic candidiasis (SC), equol treatment significantly decreased the fungal burden (liver, kidneys, and lung) in mice and local tissue damage, while enhancing the production of interleukin-10 (IL-10). Together, these findings confirm that equol is a potentially effective agent for treatment of SC.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11409501 | PMC |
http://dx.doi.org/10.1080/21505594.2024.2404256 | DOI Listing |
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