CCFM1339 Inhibits Vaginal Epithelial Barrier Injury Induced by in Mice.

The vaginal epithelial barrier, which integrates mechanical, immune, chemical, and microbial defenses, is pivotal in safeguarding against external pathogens and upholding the vaginal microecological equilibrium. Although the widely used metronidazole effectively curtails , a key pathogen in bacterial vaginosis, it falls short in restoring the vaginal barrier or reducing recurrence rates. Our prior research highlighted CCFM1339, a vaginally derived strain, for its capacity to modulate the vaginal epithelial barrier. In cellular models, CCFM1339 fortified the integrity of the cellular monolayer, augmented cellular migration, and facilitated repair. Remarkably, in animal models, CCFM1339 substantially abated the secretion of the barrier disruption biomarker E-cadherin (from 101.45 to 82.90 pg/mL) and increased the anti-inflammatory cytokine IL-10 (35.18% vs. the model), consequently mitigating vaginal inflammation in mice. Immunological assays in vaginal tissues elucidated increased secretory IgA levels (from 405.56 to 740.62 ng/mL) and curtailed gene expression. Moreover, CCFM1339 enhanced abundance and attenuated and within the vaginal microbiome, underscoring its potential in probiotic applications for vaginal barrier regulation.