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<p>Preterm pre-labor rupture of membranes (PPROM) increases maternal and neonatal sepsis risk, yet its association with maternal microbial translocation and systemic inflammation remains unclear. We investigated whether PPROM is linked to microbial DNA in maternal blood (MB) and inflammatory responses around delivery. In 66 PPROM patients (median GA: 32 weeks), MB was collected pre-delivery and within 1&#xa0;h postpartum. Fetal membranes (FM) and placental tissues were sampled immediately after delivery. Bacterial load and diversity were analyzed via 16&#xa0;S rDNA qPCR and sequencing. Maternal cytokines were quantified by multiplex immunoassay, and fetal inflammatory exposure (Triple I) assessed using histological chorioamnionitis (HCA), cord blood haptoglobin, and IL-6. Bacterial DNA was detected in maternal blood (MB) pre- and post-delivery, with a significant postpartum decline (<i>p</i> = 0.004). FM carried higher bacterial load and biodiversity than placenta (<i>p</i> &lt; 0.001), dominated by Mycoplasma spp. Maternal IL-6 and IL-10 levels rose postpartum (<i>p</i> &lt; 0.05), particularly in cases with fetal inflammatory exposure. Limited overlap was found between MB and tissue microbial taxa. In conclusion, bacterial DNA is detectable in maternal circulation in patients with PPROM before birth but rapidly clears postpartum alongside a robust cytokine surge, suggesting efficient clearance and dynamic inflammatory changes.</p>

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Rapid clearance of bacteria from maternal bloodstream after delivery in pregnancies complicated by preterm pre-labor rupture of the membranes

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月30日

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  • Catalin S. Buhimschi,
  • Guomao Zhao,
  • Kara M. Rood,
  • Lindsey Solden,
  • Shaylyn D. Webster,
  • Manel Guessas,
  • Stephanie Hearne,
  • Anthony Moussa,
  • Sonia Guessas,
  • Hongwu Jing,
  • Kathryn Berryman,
  • William E. Ackerman,
  • Irina A. Buhimschi

摘要

Preterm pre-labor rupture of membranes (PPROM) increases maternal and neonatal sepsis risk, yet its association with maternal microbial translocation and systemic inflammation remains unclear. We investigated whether PPROM is linked to microbial DNA in maternal blood (MB) and inflammatory responses around delivery. In 66 PPROM patients (median GA: 32 weeks), MB was collected pre-delivery and within 1 h postpartum. Fetal membranes (FM) and placental tissues were sampled immediately after delivery. Bacterial load and diversity were analyzed via 16 S rDNA qPCR and sequencing. Maternal cytokines were quantified by multiplex immunoassay, and fetal inflammatory exposure (Triple I) assessed using histological chorioamnionitis (HCA), cord blood haptoglobin, and IL-6. Bacterial DNA was detected in maternal blood (MB) pre- and post-delivery, with a significant postpartum decline (p = 0.004). FM carried higher bacterial load and biodiversity than placenta (p < 0.001), dominated by Mycoplasma spp. Maternal IL-6 and IL-10 levels rose postpartum (p < 0.05), particularly in cases with fetal inflammatory exposure. Limited overlap was found between MB and tissue microbial taxa. In conclusion, bacterial DNA is detectable in maternal circulation in patients with PPROM before birth but rapidly clears postpartum alongside a robust cytokine surge, suggesting efficient clearance and dynamic inflammatory changes.