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Distal pulmonary epithelial maturation in preterm infants: does the lung of the preterm infant continue its
Raluca Chirculescu1,2, Paul Cristian Balanescu1,3, Gheorghe Peltecu1,4
1Carol Davila University of Medicine and Pharmacy, Bucharest, Romania.
Insights
Premature birth causes respiratory distress due to immature lungs. This study found surfactant present in all preterm neonates, with Napsin A expression linked to factors promoting lung maturation.
Area of Science:
- Neonatology
- Pulmonary Medicine
- Developmental Biology
Background:
- Premature birth disrupts lung development, leading to respiratory distress syndrome (RDS) due to surfactant deficiency.
- RDS severity increases with extreme prematurity, highlighting the need to understand pulmonary maturation.
- Functional pulmonary maturation is crucial for neonatal respiratory health.
Purpose of the Study:
- To evaluate the presence and patterns of postnatal pulmonary functional maturation in preterm neonates.
- To investigate the expression of surfactant and Napsin A in the pulmonary tissue of preterm infants.
- To correlate marker expression with prenatal and postnatal factors.
Main Methods:
- Immunohistochemical assays for surfactant and Napsin A were performed on pulmonary tissue from 67 preterm neonates (23-35 weeks gestational age).
- Tissue microarrays (5 micrometers) were analyzed using optical microscopy.
- Marker expression in the distal lung epithelium was correlated with gestational age, lifespan, oxygen therapy, mechanical ventilation, antenatal corticosteroids, and maternal infections.
Main Results:
- Surfactant was detected in the pulmonary tissue of all neonates, irrespective of gestational age or lifespan.
- Napsin A expression intensity positively correlated with gestational age, duration of oxygen therapy/mechanical ventilation, antenatal corticosteroid administration, and maternal infections.
- Mechanical ventilation and antenatal interventions appear to promote pulmonary function and surfactant production.
Conclusions:
- All studied preterm neonates exhibited surfactant, indicating its presence even with immature lungs.
- Napsin A expression serves as a marker for pulmonary maturation influenced by mechanical ventilation, antenatal corticosteroids, and maternal infections.
- These factors enhance lung function and surfactant production, crucial for managing respiratory distress in premature infants.
Abstract:
Disruption of pulmonary development caused by premature birth before the achievement of functional pulmonary maturation culminates in respiratory distress syndrome, primarily due to surfactant deficiency. Furthermore, the severity of this syndrome intensifies, particularly in the case of extremely premature neonates. This investigation aimed to evaluate the presence of postnatal pulmonary functional maturation in premature neonates. In pursuit of this objective, we conducted immunohistochemical assays for surfactant and Napsin A within the pulmonary tissue of 67 preterm neonates, with gestational ages ranging from 23 to 35 weeks, whose lifespans varied between one day and 149 days. The two immunohistochemical markers were evaluated within the pulmonary distal epithelium, and their expression was interpreted in relation to various pre- and postnatal factors. The examination was performed on tissue microarrays, sectioned at 5 micrometers, and the assessment of the immunohistochemical markers was interpreted from photographs captured under the optical microscope. Our investigation revealed that all neonates, regardless of their gestational age or lifespan, demonstrated the presence of surfactant within the pulmonary tissue. The intensity of Napsin A expression exhibited a positive correlation with gestational age, duration of oxygen therapy/mechanical ventilation, administration of antenatal corticosteroids, and maternal infections during pregnancy. In summary, our research demonstrated that mechanical ventilation, through the dynamic process of alveolar distension, promotes surfactant production within the distal lung epithelium. Antenatal treatment with corticosteroids and maternal antenatal infections enhances pulmonary function, facilitating surfactant production.
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