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Updated: Aug 4, 2025

A Murine Model of Fetal Exposure to Maternal Inflammation to Study the Effects of Acute Chorioamnionitis on Newborn Intestinal Development
Published on: June 24, 2020
The role of interleukin-1 in perinatal inflammation and its impact on transitional circulation
Josephine C Owen1,2, Steven P Garrick1,2, Briana M Peterson1,2
1Ritchie Centre, Hudson Institute of Medical Research, Melbourne, VIC, Australia.
Insights
Preterm birth complications can impair infant circulatory transition. Targeting interleukin-1 (IL-1) inflammation shows promise for improving outcomes in premature infants born due to chorioamnionitis or fetal growth restriction.
Area of Science:
- Neonatal Physiology
- Perinatal Medicine
- Immunology
Background:
- Preterm birth (<37 weeks gestational age) affects millions globally, increasing risks of early life diseases.
- Improved survival in extremely premature infants is linked to higher incidence of short- and long-term morbidities.
- The transition from fetal to neonatal circulation is critical and can be impaired by conditions like chorioamnionitis and fetal growth restriction (FGR).
Purpose of the Study:
- To outline mechanistic pathways of impaired circulatory transition in preterm infants.
- To explore the role of interleukin-1 (IL-1) in chorioamnionitis and FGR-related circulatory abnormalities.
- To investigate the therapeutic potential of targeting IL-1 for improving perinatal circulatory transition.
Main Methods:
- Review of mechanistic pathways linking chorioamnionitis and FGR to circulatory transition abnormalities.
- Analysis of the role of pro-inflammatory cytokines, particularly IL-1, in perinatal inflammation.
- Exploration of preclinical findings on the efficacy of anti-inflammatory strategies targeting IL-1.
Main Results:
- Maternal chorioamnionitis and fetal growth restriction (FGR) are common causes of preterm birth associated with impaired circulatory transition.
- Interleukin-1 (IL-1) plays a central role in the pathogenesis of chorioamnionitis-related perinatal inflammatory diseases.
- Inflammation, potentially mediated by IL-1, is implicated in FGR and in-utero hypoxia, affecting circulatory adaptation.
Conclusions:
- Abnormalities in transitional circulation are linked to common preterm birth causes like chorioamnionitis and FGR.
- Targeting IL-1-driven inflammation presents a promising therapeutic strategy for improving circulatory transition in at-risk preterm infants.
- Early and effective anti-inflammatory interventions hold potential for mitigating short- and long-term sequelae of impaired perinatal adaptation.
Abstract:
Preterm birth is defined as delivery at <37 weeks of gestational age (GA) and exposes 15 million infants worldwide to serious early life diseases. Lowering the age of viability to 22 weeks GA entailed provision of intensive care to a greater number of extremely premature infants. Moreover, improved survival, especially at extremes of prematurity, comes with a rising incidence of early life diseases with short- and long-term sequelae. The transition from fetal to neonatal circulation is a substantial and complex physiologic adaptation, which normally happens rapidly and in an orderly sequence. Maternal chorioamnionitis or fetal growth restriction (FGR) are two common causes of preterm birth that are associated with impaired circulatory transition. Among many cytokines contributing to the pathogenesis of chorioamnionitis-related perinatal inflammatory diseases, the potent pro-inflammatory interleukin (IL)-1 has been shown to play a central role. The effects of utero-placental insufficiency-related FGR and in-utero hypoxia may also be mediated, in part, via the inflammatory cascade. In preclinical studies, blocking such inflammation, early and effectively, holds great promise for improving the transition of circulation. In this mini-review, we outline the mechanistic pathways leading to abnormalities in transitional circulation in chorioamnionitis and FGR. In addition, we explore the therapeutic potential of targeting IL-1 and its influence on perinatal transition in the context of chorioamnionitis and FGR.
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