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Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats
Published on: November 20, 2015
[Effect of perinatal inflammation syndrome on lung maturation and development]
T Lacaze-Masmonteil1, B Thébaud
1Pédiatrie et Réanimation Néonatales, Hôpital Antoine-Béclère, AP/HP, 157, rue de la Porte-de-Trivaux, 92141 Clamart.
Insights
Inflammation in newborns may cause chronic lung disease, even without ventilation. Understanding this link is key to developing new treatments for very preterm infants and preventing bronchopulmonary dysplasia.
Area of Science:
- Neonatal Medicine
- Pulmonology
- Immunology
Context:
- Bronchopulmonary dysplasia (BPD) incidence remains high despite advances in neonatal care.
- Chronic lung disease affects very premature infants, even those not requiring mechanical ventilation.
- Inflammation, triggered prenatally or perinatally, is increasingly linked to chronic lung disease development.
Purpose:
- To review evidence linking inflammation to chronic lung disease in neonates.
- To explore the dual role of inflammatory mediators in lung maturation.
- To identify knowledge gaps regarding inflammation's impact on alveolarization.
Summary:
- Epidemiological, experimental, and clinical data suggest inflammation is a key factor in developing chronic lung disease.
- Proinflammatory mediators can paradoxically aid lung maturation, complicating direct therapeutic targeting.
- Further research is needed to elucidate how inflammation affects lung maturation and alveolar development.
Impact:
- Highlights the critical role of the inflammatory response in neonatal chronic lung disease.
- Suggests potential for novel immunomodulatory therapies to prevent lung disease in preterm infants.
- Emphasizes the need for a nuanced understanding of inflammation's effects on developing lungs.
Abstract:
Despite improvement in neonatal care, the incidence of bronchopulmonary dysplasia has not decreased over the last decade. Moreover, chronic lung disease still occurs in very premature infants who do not require ventilatory support at birth. This review presents the growing body of epidemiological, experimental and clinical evidence suggesting that the occurrence of an inflammatory reaction triggered in utero or immediately after birth is associated with the subsequent development of chronic lung disease. However, stimulators of inflammation or specific proinflammatory cytokines may also have beneficial on lung maturation. How proinflammatory mediators interfere with lung maturation and alveolarization needs to be better understood in order to pave the way for new immunomodulatory strategies to prevent chronic lung disease in very preterm infants.
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