Premature birth is a major risk factor for infection in infants and long-term functional defects in the lung. However, how premature birth affects the composition and function of human airway epithelium remains elusive. To address this critical question, we have established a robust methodology of epithelial basal stem cell derivation from tracheal aspirate samples collected from intubated preterm and term newborns. This project aims to identify molecular pathways that are associated with preterm birth and affects basal stem cell differentiation and the barrier function of differentiated airway epithelial cells. A clinically relevant disease model is infection of preterm airway epithelial cells by respiratory syncytial virus.
