ArticleBMC microbiology2025
D-lactic acid inhibits Candida albicans associated with vulvovaginal candidiasis: in vitro and in vivo effects and underlying mechanisms.
Article in BMC microbiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundCandida albicans (C. albicans) is a major opportunistic fungal pathogen responsible for both invasive and superficial infections, including vulvovaginal candidiasis (VVC), which affects a large proportion of women worldwide and is prone to recurrence. Limitations of conventional antifungal therapies and the emergence of drug resistance highlight the urgent need for novel therapeutic agents. D-lactic acid (D-LA), a chiral organic acid naturally produced by Lactobacillus spp., has been proposed as a potential antifungal candidate. However, its activity against C. albicans and underlying mechanisms remain unclear. Therefore, this study aimed to evaluate the antifungal activity of D-LA against C. albicans and to explore its potential mechanisms.
methodsC. albicans SC5314 was treated with D-LA in vitro to evaluate its effects on fungal growth, hyphal morphogenesis, and biofilm development using broth microdilution assays, hyphal induction/inhibition assays, crystal violet staining, and XTT-based metabolic activity measurement. Cell membrane integrity was assessed via trypan blue exclusion and live/dead fluorescent staining. RNA-seq and qRT-PCR were performed to identify differentially expressed genes and enriched functional pathways. The antifungal efficacy of D-LA was further evaluated in a mouse model of vaginal candidiasis.
resultsD-LA significantly inhibited hyphal formation and biofilm development in a concentration-dependent manner. Crystal violet and XTT assays confirmed substantial suppression of biofilm biomass and metabolic activity. Live/dead staining and trypan blue exclusion indicated increased cell membrane damage after D-LA exposure. Transcriptomic profiling revealed significant changes in genes related to hyphal development, cell wall organization, iron metabolism, acid phosphatase activity, and stress response. qRT-PCR validation demonstrated that the addition of D-LA downregulated virulence-associated genes (ECE1, TEC1, ALS1) and upregulated the pH-regulated gene PHR2 in C. albicans. Cytotoxicity testing on VK2/E6E7 vaginal epithelial cells indicated minimal toxicity at concentrations effective against C. albicans. In vivo antifungal efficacy and safety of D-LA in a mouse model of C. albicans vaginal infection demonstrating potent efficacy and a favorable profile.
conclusionD-LA exhibits potent antifungal activity against C. albicans by disrupting hyphal formation, biofilm development, and cell wall integrity, accompanied by transcriptional reprogramming of virulence-associated pathways. Its low cytotoxicity towards vaginal epithelial cells and mouse vaginal mucosa supports its potential as a safe alternative or adjunctive agent for VVC management.
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