Pediatric researchers have identified a key component of the pathogenesis of bronchopulmonary dysplasia (BPD), a lung disease that affects premature infants.
Bronchopulmonary dysplasia, a common chronic lung disease in premature infants, develops as a result of the ventilation and oxygen necessary for these infants to survive. Infants born before 30 weeks gestation have immature lungs that lack surfactant, a substance comprised of phospholipids and proteins that is needed for lungs to properly function. This causes premature infants to develop respiratory distress syndrome, requiring the aid of mechanical ventilation. The infants’ exposure to elevated oxygen levels during ventilation activates the process of inflammation that leads to BPD.
“The same ventilation that ultimately saves their lives, damages their lungs,” said Dr Rashmin Savani, professor and chief of Neonatal-Perinatal Medicine, and senior author of the study. “Our findings suggest that if we target premature infants born at less than 28 weeks gestation from three to 10 days after birth with this therapy, we might be able to drastically reduce or even eliminate the development of BPD.”
To confirm NLRP3’s role in regulating the inflammatory process of BPD, researchers used neonatal animal models exposed to 85% oxygen, which is a key cause of the inflammation and decreased development of tiny air sacs in the lungs called alveoli. They also examined tracheal aspirate samples from premature infants to establish the importance of the NLRP3 inflammasome in the development of BPD.
Photo Credit: UT Southwestern Medical Center
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