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<p>Labor induction failure increases the risk of unplanned cesarean delivery and maternal-neonatal complications. However, the determinants of induction sensitivity remain poorly understood. In this prospective cohort of 85 term pregnant women undergoing labor induction with Propess® (prostaglandin E2), we combined full-length 16S rRNA sequencing of the vaginal microbiota, untargeted metabolomics of vaginal secretions, and transcriptomic analysis of cervical stromal cells exposed to <i>Lactobacillus crispatus</i> supernatant to identify predictive factors and underlying mechanisms. We found that women with a poor induction response exhibited higher vaginal microbiota α-diversity and a significant reduction in <i>L. crispatus</i> abundance. The relative abundance of <i>L. crispatus</i> predicted induction success with an area under the curve (AUC) of 0.80 (95% CI: 0.70–0.90). Metabolomic analysis revealed distinct vaginal metabolic alterations in induction-insensitive women. Importantly, in vitro experiments showed that <i>L. crispatus</i> supernatant directly modulates the transcriptome of cervical stromal cells, upregulating genes involved in uterine contraction, tissue remodeling, and immune regulation. Our results identify vaginal <i>L. crispatus</i> as a key biomarker for labor induction sensitivity and elucidate a potential mechanism by which it primes the cervix for prostaglandin response. These findings provide a novel microbiota–host interaction framework for personalizing induction strategies in precision obstetrics.</p>

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A microbiota–host axis mediates prostaglandin sensitivity: Lactobacillus crispatus as a biomarker and regulator of human labor induction

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年3月17日

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  • Zizhuo Wang,
  • Weidong Tan,
  • Zhenzhen He,
  • Liangnan Zhang,
  • Yilin Fu,
  • Nary Long,
  • Phannaroat Sourn,
  • Weikun Li,
  • Junjie Yuan,
  • Yuxin Chen,
  • Huihui Yu,
  • Wanjiang Zeng,
  • Ling Feng,
  • Jianli Wu,
  • Shaoshuai Wang,
  • Wencheng Ding

摘要

Labor induction failure increases the risk of unplanned cesarean delivery and maternal-neonatal complications. However, the determinants of induction sensitivity remain poorly understood. In this prospective cohort of 85 term pregnant women undergoing labor induction with Propess® (prostaglandin E2), we combined full-length 16S rRNA sequencing of the vaginal microbiota, untargeted metabolomics of vaginal secretions, and transcriptomic analysis of cervical stromal cells exposed to Lactobacillus crispatus supernatant to identify predictive factors and underlying mechanisms. We found that women with a poor induction response exhibited higher vaginal microbiota α-diversity and a significant reduction in L. crispatus abundance. The relative abundance of L. crispatus predicted induction success with an area under the curve (AUC) of 0.80 (95% CI: 0.70–0.90). Metabolomic analysis revealed distinct vaginal metabolic alterations in induction-insensitive women. Importantly, in vitro experiments showed that L. crispatus supernatant directly modulates the transcriptome of cervical stromal cells, upregulating genes involved in uterine contraction, tissue remodeling, and immune regulation. Our results identify vaginal L. crispatus as a key biomarker for labor induction sensitivity and elucidate a potential mechanism by which it primes the cervix for prostaglandin response. These findings provide a novel microbiota–host interaction framework for personalizing induction strategies in precision obstetrics.