Host-microbiome interactions in distinct subsets of preterm labor and birth

Jose Galaz, Roberto Romero, Jonathan M. Greenberg, Kevin R. Theis, Marcia Arenas-Hernandez, Yi Xu, Marcelo Farias-Jofre, Derek Miller, Tomi Kanninen, Valeria Garcia-Flores, Nardhy Gomez-Lopez

Research output: Contribution to journalArticlepeer-review

2 Scopus citations

Abstract

Preterm birth, the leading cause of perinatal morbidity, often follows premature labor, a syndrome whose prevention remains a challenge. To better understand the relationship between premature labor and host-microbiome interactions, we conducted a mechanistic investigation using three preterm birth models. We report that intra-amniotic delivery of LPS triggers inflammatory responses in the amniotic cavity and cervico-vaginal microenvironment, causing vaginal microbiome changes and signs of active labor. Intra-amniotic IL-1α delivery causes a moderate inflammatory response in the amniotic cavity but increasing inflammation in the cervico-vaginal space, leading to vaginal microbiome disruption and signs of active labor. Conversely, progesterone action blockade by RU-486 triggers local immune responses accompanying signs of active labor without altering the vaginal microbiome. Preterm labor facilitates ascension of cervico-vaginal bacteria into the amniotic cavity, regardless of stimulus. This study provides compelling mechanistic insights into the dynamic host-microbiome interactions within the cervico-vaginal microenvironment that accompany premature labor and birth.

Original languageEnglish
Article number108341
JournaliScience
Volume26
Issue number12
DOIs
StatePublished - Dec 15 2023

Keywords

  • Cell
  • Microbiome
  • Women's health

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