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Published on: May 4, 2020
Lung development and function in preterm infants in the surfactant treatment era
1Pulmonary Biology/Neonatology, Children's Hospital Medical Center, Cincinnati, Ohio 45229, USA. JOBEAO@CHMCC.ORG
Insights
Advances in neonatal care have reduced infant mortality for low birth weight infants. However, chronic lung disease remains a challenge, with new research questioning traditional views on lung development and glucocorticoid treatments.
Area of Science:
- Neonatal Medicine
- Pulmonary Biology
- Developmental Pediatrics
Background:
- Neonatal intensive care advances have decreased mortality in infants under 1-kg birth weight.
- Despite improved survival, many extremely preterm infants develop chronic lung disease, marked by impaired lung development and alveolarization.
- Current understanding of antenatal glucocorticoid effects on lung maturation is being re-evaluated based on new experimental data.
Purpose of the Study:
- To investigate the mechanisms underlying chronic lung disease in very preterm infants.
- To explore the role of antenatal glucocorticoids and proinflammatory cytokines in lung development and injury.
- To examine potential differences in lung injury mechanisms between developing and adult lungs.
Main Methods:
- Review of recent findings from transgenic and experimental models.
- Analysis of clinical data on surfactant, antenatal glucocorticoid treatments, and ventilation strategies.
- Investigation of the impact of antenatal proinflammatory exposures and postnatal injury on lung development.
Main Results:
- Traditional explanations for antenatal glucocorticoid effects on developing lungs are insufficient.
- Very preterm infants' lungs are vulnerable to ventilation-induced injury due to small gas volumes and delicate tissue.
- Proinflammatory cytokines may influence both lung development and injury, with potential unique mechanisms in the developing lung.
Conclusions:
- Chronic lung disease in very preterm infants necessitates a deeper understanding beyond current therapeutic paradigms.
- Further research into the complex interplay of inflammation, glucocorticoids, and mechanical ventilation is crucial for improving outcomes.
- Investigating developmental-specific mechanisms of lung injury is essential for targeted therapeutic strategies.
Abstract:
Mortality of infants of < 1-kg birth weight has decreased because of surfactant treatments, antenatal glucocorticoid treatments, and new ventilation strategies. However, many of these infants develop a chronic lung disease characterized by an arrest of lung development and interference with alveolarization. Antenatal glucocorticoids can induce early lung maturation clinically, but new information from transgenic and other experimental models indicates that traditional explanations for glucocorticoid effects on the developing lung are inadequate. These very preterm infants have lungs with small lung gas volumes and delicate lung tissue that are susceptible to injury with the initiation of ventilation and subsequent ventilation. Antenatal proinflammatory exposures are frequent in very preterm infants, and postnatal injury is associated with elevations of proinflammatory cytokines in the lungs. One hypothesis is that proinflammatory cytokines can promote or interfere with lung development as well as promote lung injury. Mechanisms of lung injury being characterized in the adult lung may have unique characteristics in the developing lung.
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