Abstract
(1) Background: Candida is the most common cause of fungal infections worldwide, but due to the limited option of antifungal therapies, alternative strategies are required. (2) Methods: Adenophora triphylla var. japonica extract was used for the biofilm formation assay using RPMI1640. The combinatorial antifungal assay, the dimorphic transition assay, and the adherence assay were done to see the influence of inhibition of biofilm formation. qRT-PCR analysis were performed to check the gene expression. (3) Results: Adenophora triphylla var. japonica extract inhibited the Candida biofilm formation. Treatment of extract increased the antifungal susceptibility of miconazole from a 37% reduction in fungal growth to 99.05%, and also dose-dependently reduced the dimorphic transition of Candida and the attachment of Candida to HaCaT cells. The extract blocked the expression of hyphal-related genes, extracellular matrix genes, Ras1-cAMP-PKA pathway genes, Cph2-Tec1 pathway gene, and MAP kinase pathway gene. (4) Conclusions: In this study, the treatment of Adenophora triphylla var. japonica extract showed inhibition of fungal biofilm formation, activation of antifungal susceptibility, and reduction of infection. These results suggest that fungal biofilm formation is a good target for the development of antifungal adjuvants, and Adenophora triphylla var. japonica extract should be a good candidate for biofilm-associated fungal infections.
Highlights
Japonica extract should be a good candidate for biofilm-associated fungal infections
Some antifungal agents inhibit fungal biofilm formation because they kill fungi and growth of C. albicans after 24 h incubation
A. triphylla var. japonica extract did not affect the tion of biofilm formation was not due to the reduced growth of Candida
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. Candida albicans is an opportunistic fungal pathogen that can cause systemic infections in individuals when mucosal barriers are disrupted, or the immune system is compromised [1]. Nosocomial C. albicans infection is often linked with the ability to form biofilms on mucosal surfaces and implanted medical devices [1,2,3]. Biofilm formation is a finely regulated process by multiple interconnected signaling pathways [4,5,6,7,8] and causes structured microbial communities to attach to surfaces [9,10]
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