Abstract:
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 Gardnerella vaginalis, a key pathogen in bacterial vaginosis, it falls short in restoring the vaginal barrier or reducing recurrence rates. Our prior research highlighted Lactobacillus crispatus CCFM1339, a vaginally derived Lactobacillus strain, for its capacity to modulate the vaginal epithelial barrier. In cellular models, L. crispatus CCFM1339 fortified the integrity of the cellular monolayer, augmented cellular migration, and facilitated repair. Remarkably, in animal models, L. crispatus 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 IL-17 gene expression. Moreover, L. crispatus CCFM1339 enhanced Lactobacilli abundance and attenuated Enterobacterium and Enterococcus within the vaginal microbiome, underscoring its potential in probiotic applications for vaginal barrier regulation.
摘要:
阴道上皮屏障,它集成了机械,免疫,化学,和微生物防御,在抵御外部病原体和维护阴道微生态平衡方面至关重要。尽管广泛使用的甲硝唑有效地减少了阴道加德纳菌,细菌性阴道病的关键病原体,它不足以恢复阴道屏障或降低复发率。我们之前的研究强调了卷曲乳杆菌CCFM1339,一种阴道来源的乳杆菌,调节阴道上皮屏障的能力。在细胞模型中,L.crispatusCCFM1339加强了细胞单层的完整性,增强的细胞迁移,促进修复。值得注意的是,在动物模型中,L.crispatusCCFM1339大大减少了屏障破坏生物标志物E-cadherin的分泌(从101.45到82.90pg/mL),并增加了抗炎细胞因子IL-10(35.18%vs.模型),从而减轻小鼠的阴道炎症。阴道组织中的免疫学测定阐明了分泌性IgA水平的增加(从405.56到740.62ng/mL)并减少了IL-17基因的表达。此外,卷曲乳杆菌CCFM1339增强了乳杆菌的丰度,并减毒了阴道微生物群内的肠杆菌和肠球菌,强调其在益生菌应用于阴道屏障调节方面的潜力。