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Published on: October 31, 2025
Acute lung injury in preterm fetuses and neonates: mechanisms and molecular pathways
Zoe Iliodromiti1, Dimitrios Zygouris, Stavros Sifakis
12nd Department of Obstetrics and Gynecology, University of Athens Medical School, Aretaieio Hospital , Athens , Greece .
Insights
Acute lung injury (ALI) in preterm neonates is a serious condition caused by inflammation. Understanding these inflammatory pathways is key to developing new treatments for prevention and resolution.
Area of Science:
- Neonatal Medicine
- Pulmonology
- Inflammation Research
Background:
- Acute lung injury (ALI) significantly impacts preterm neonates, leading to high morbidity and mortality.
- ALI involves damage to the fetal lung's alveolar-capillary unit and cellular linings due to inflammatory responses.
- Key triggers include chorioamnionitis and mechanical ventilation, which induce proinflammatory cytokines.
Purpose of the Study:
- To explore the inflammatory pathways linking intra-amniotic inflammation and ALI in preterm neonates.
- To identify potential targets for novel interventional procedures.
- To guide future research on ALI pathophysiology and pharmaceutical interventions.
Main Methods:
- Review of existing literature on ALI pathogenesis in preterm neonates.
- Analysis of inflammatory mediators (e.g., TNF-α, IL-1, IL-6, VEGF) involved in lung injury.
- Examination of the role of chorioamnionitis, mechanical ventilation, and reactive oxygen species (ROS).
Main Results:
- Inflammatory cytokines and products damage capillary endothelium and alveolar epithelium, causing hyaline membrane formation and alveolar edema.
- Mechanical ventilation and hyperoxia-induced ROS contribute to ALI by increasing proinflammatory cytokines and tissue injury.
- Chorioamnionitis is a major factor in initiating fetal lung inflammation.
Conclusions:
- Understanding the inflammatory cascade connecting intra-amniotic inflammation and ALI is crucial for developing preventative strategies.
- Further research into the pathophysiology of ALI and potential pharmaceutical interventions is warranted for preterm neonates.
- Targeting inflammatory pathways offers a promising avenue for managing and treating ALI in this vulnerable population.
Abstract:
Acute lung injury (ALI) results in high morbidity and mortality among preterm neonates and efforts have therefore been devoted to both antenatal and postnatal prevention of the disease. ALI is the result of an inflammatory response which is triggered by a variety of different mechanisms. It mostly affects the fetal lung and, in particular, causes damage to the integrity of the lung's alveolar-capillary unit while weakening its cellular linings. Chemotactic activity and inflammatory products, such as proinflammatory cytokines TNF-α, IL-1, IL-6, IL-11, VEGF,TGF-α and TGF-β, provoke serious damage to the capillary endothelium and the alveolar epithelium, resulting in hyaline membrane formation and leakage of protein-rich edema fluid into the alveoli. Chorioamnionitis plays a major part in triggering fetal lung inflammation, while mechanical ventilation, the application of which is frequently necessary in preterm neonates, also causes ALI by inducing proinflammatory cytokines. Many different ventilation-strategies have been developed in order to reduce potential lung injury. Furthermore, tissue injury may occur as a result of injurious oxygen by-products (Reactive Oxygen Species, ROS), secondary to hyperoxia. Knowledge of the inflammatory pathways that connect intra-amniotic inflammation and ALI can lead to the formulation of novel interventional procedures. Future research should concentrate on the pathophysiology of ALI in preterm neonates and οn possible pharmaceutical interventions targeting prevention and/or resolution of ALI.
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