Effect of Lactobacillus.salivarius HHuMin-U on gene expression of VK2/E6E7 juman 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-?B 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. Overall design: To investigate the effects of Lactobacillus salivarius HHuMin-U (HMU) on vaginal epithelial cells, VK2/E6E7 cells were seeded and divided into two groups. Control: PBS-treated; HMU: HMU-treated at a concentration of 1×10^8 CFU/mL. Cells were treated with PBS or HMU for 6 hours before total RNA was extracted using the RNeasy Mini Kit (Qiagen, Hilden, Germany). Three biological replicates were prepared for each group.