A recent study published in the British Journal of Pharmacology and conducted by a team of Italian researchers led by Luca Filippi, Associate Professor of General and Specialist Paediatrics at the University of Pisa and Head of the Neonatology Unit at the Azienda Ospedaliero-Universitaria Pisana (Aoup), together with Alessandro Pini (University of Florence), has identified a new mechanism for protecting the lungs of premature infants at risk of developing bronchopulmonary dysplasia (BPD), the most severe chronic respiratory disease affecting extremely preterm newborns.
This condition primarily affects infants who require prolonged mechanical ventilation with high concentrations of oxygen. While life-saving, extended exposure to high oxygen levels can damage immature lungs, causing oxidative stress, disrupting normal alveolar development and reducing the number of blood vessels, all factors that can severely compromise respiratory function.
In their study, which also involved the Department of Chemistry and Industrial Chemistry of the University of Pisa, the IRCCS Meyer Children’s Hospital, and the National Institute of Optics (CNR) in Sesto Fiorentino, the researchers demonstrated that activation of the β3-adrenergic receptor — a protein that is naturally regulated by oxygen levels — can protect the lungs from the harmful effects of hyperoxia. In an experimental model of bronchopulmonary dysplasia in neonatal rats, treatment with a β3-receptor agonist significantly reduced oxidative stress, preserved lung and vascular tissue structure, and limited the development of fibrosis.
In particular, the treatment improved the development of alveoli and the pulmonary vascular network, with a significant impact on survival: at the most effective dose, the survival rate of treated animals was approximately twice that of untreated subjects.
This research is part of a broader and more ambitious scientific project aimed at reproducing, even after birth, the protective benefits normally provided by the maternal womb through targeted pharmacological interventions. The researchers have described this approach as a “pharmacological artificial placenta”, designed to protect the immature organs of premature infants from the effects of the extrauterine environment, particularly from excessive oxygen exposure.
This strategy is supported by the fact that encouraging results have already been observed in other organs that are particularly vulnerable in preterm infants, such as the retina, the intestine and the nervous system. These findings suggest that pharmacological stimulation of the β3-adrenergic receptor may offer systemic protection against hyperoxia-induced damage. Although further studies are needed before these results can be put into practice in humans, the findings open up new avenues for the development of innovative and more physiological therapies. The ultimate goal is to improve both survival rates and quality of life for babies born too soon.
