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Antenatal factors and the development of bronchopulmonary dysplasia
1Division of Pulmonary Biology, Cincinnati Children's Hospital, 3333 Burnet Avenue, 45229-3039, Cincinnati,OH, USA. alan.jobe@chmcc.org
Insights
Bronchopulmonary dysplasia may result from repeated lung injuries. Antenatal glucocorticoids and intra-uterine inflammation are identified as potential initial insults contributing to this condition in preterm infants.
Area of Science:
- Neonatal respiratory research
- Fetal lung development
- Pediatric pulmonology
Background:
- Preterm fetal lungs face antenatal glucocorticoid exposure and frequent histologic chorioamnionitis.
- While associated with early lung maturation, these factors decrease alveolarization in experimental models.
- Antenatal inflammation can worsen lung inflammation from mechanical ventilation in preterm infants.
Purpose of the Study:
- To hypothesize that bronchopulmonary dysplasia arises from repetitive adverse lung exposures (hits).
- To identify antenatal glucocorticoid exposure and/or antenatal inflammation as potential initial hits.
- To explore the multifactorial etiology of bronchopulmonary dysplasia.
Main Methods:
- Review of clinical and experimental data on antenatal factors and preterm lung development.
- Analysis of the impact of glucocorticoids and chorioamnionitis on alveolarization.
- Examination of the interaction between antenatal inflammation and mechanical ventilation.
Main Results:
- Antenatal glucocorticoids and chorioamnionitis are linked to early lung maturation.
- Both factors reduce alveolarization in experimental settings.
- Chorioamnionitis exacerbates the preterm lung's inflammatory response to ventilation.
Conclusions:
- Bronchopulmonary dysplasia is proposed to result from cumulative lung insults.
- Antenatal glucocorticoid exposure and intra-uterine inflammation are hypothesized as primary contributors.
- Understanding these initial hits is crucial for preventing bronchopulmonary dysplasia.
Abstract:
The lung of the preterm fetus is often exposed to antenatal glucocorticoids, and histologic chorioamnionitis is frequent. Clinically and experimentally, antenatal glucocorticoids and/or chorioamnionitis are associated with early lung maturation, but in experimental models, both glucocorticoids and intra-uterine inflammation decrease alveolarization. Experimental chorioamnionitis also can amplify the inflammatory response of the preterm lung to mechanical ventilation. In this article, the hypothesis developed is that bronchopulmonary dysplasia occurs because of repetitive adverse lung exposures, or hits, and that the initial hits may be antenatal glucocorticoid exposure and/or antenatal inflammation.