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Updated: Jun 7, 2026
Modeling Ascending Vaginal Infection, Preterm Birth, and Neonatal Morbidity in Mice
Published on: October 10, 2025
Novel insights into molecular mechanisms of abruption-induced preterm birth
Catalin S Buhimschi1, Frederik Schatz, Graciela Krikun
1Department of Obstetrics, Gynecology and Reproductive Sciences, Yale University School of Medicine, New Haven, CT 06520, USA. catalin.buhimschi@yale.edu
Insights
Preterm birth (PTB) is a major complication in deliveries. This study reveals how placental abruption, via thrombin, triggers inflammation and contributes to PTB.
Area of Science:
- Reproductive Biology
- Obstetrics
- Immunology
Background:
- Preterm birth (PTB) affects over 12% of deliveries, with its causes often unknown.
- Intra-amniotic infection and decidual hemorrhage (abruption) are key PTB antecedents with shared pathways.
- High-dimensional technologies reveal crosstalk between coagulation and inflammation pathways.
Purpose of the Study:
- To elucidate molecular mechanisms linking placental abruption to preterm birth.
- To investigate the role of coagulation and inflammation crosstalk in PTB.
Main Methods:
- Analysis of high-throughput, high-dimensional data.
- Examination of molecular mediators such as tissue factor, thrombin, and cytokines.
Main Results:
- Placental abruption is linked to excessive thrombin generation.
- Thrombin promotes inflammation-associated PTB by increasing matrix metalloproteinase and chemokine expression.
- Tissue factor, thrombin, and cytokines are key mediators of pathway crosstalk.
Conclusions:
- Thrombin plays a dual role in coagulation and inflammation, contributing to PTB in abruption settings.
- Novel insights into PTB mechanisms driven by placental abruption are provided.
Abstract:
Preterm birth (PTB) complicates more than 12% of all deliveries. Despite significant research, the aetiology of most cases of PTB remains elusive. Two major antecedents of PTB, intra-amniotic infection and decidual haemorrhage (abruption), can exhibit dissimilar demographic and genetic predispositions, despite sharing common molecular and cellular pathways. The use of high-throughput, high-dimensional technologies reveals substantial crosstalk between the coagulation and inflammation pathways. Tissue factor, thrombin and cytokines are key mediators of this crosstalk. Abruptions are associated with excess thrombin generated from decidual-cell-expressed tissue factor. Although thrombin is a primary mediator of the coagulation cascade, it can also promote inflammation-associated PTB by enhancing expression of matrix metalloproteinase and neutrophil-chemoattracting and -activating chemokines. Here, we provide novel insights into the molecular mechanisms and pathways leading to PTB in the setting of placental abruption.
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