Effect of Lactobacillus salivarius HHuMin-U on gene expression of VK2/E6E7 human vaginal cell lines.

Vulvovaginal candidiasis (VVC) is a common mucosal infection caused by Candida albicans, characterized by inflammation and disruption of epithelial immunity. Probiotic therapy has emerged as a promising approach for managing VVC by modulating host immune responses and enhancing mucosal defenses. In this study, we investigated the therapeutic potential of Lactobacillus salivarius HHuMin-U (HMU) against VVC using in vitro and in vivo models. HMU treatment enhanced the expression of antimicrobial peptides (AMPs) such as DEFB1 and S100A8 and modulated cytokine production (e.g., IL-6, IL-8) in vaginal epithelial cells. Furthermore, RNA sequencing of HMU-treated VK2/E6E7 cells revealed significant transcriptional changes, including upregulation of epithelial barrier function and immune-enhancing pathways. Gene Set Enrichment Analysis (GSEA) identified the NF-κB pathway as a critical regulator of HMU-induced immunity. In vivo, HMU administration significantly reduced fungal burden, mitigated tissue inflammation, and improved epithelial integrity in a murine model of VVC. The sequencing data presented in this report provide a comprehensive transcriptomic landscape of HMU-treated vaginal epithelial cells and offer insights into its underlying mechanisms. These findings support the therapeutic potential of HMU as a probiotic agent for VVC management.