Randomized trial observes compromised lung barrier function in infants with bronchopulmonary dysplasia, suggesting new therapeutic targets.
Key Points
This research aims to characterize the cellular and transcriptomic landscape of the lungs in bronchopulmonary dysplasia (BPD) to identify dysfunctions.
Analyzed FFPE lung sections from 9 premature infants with BPD, 6 control premature infants, and 9 full-term infants.
Implemented genome-wide spatial transcriptomics and gene ontology enrichment analysis.
Conducted immunofluorescence on identified molecular targets for confirmation.
Significant downregulation of CC16 and cilia-associated proteins in BPD airways confirmed by immunofluorescence.
BPD lung parenchyma exhibited reduced surfactant proteins A and D with elevated antimicrobial peptides due to inflammation.
Altered cellular composition noted with fewer club and mucociliary cells, indicating potential for increased infection susceptibility.