The study, led by researchers from the the University of Rochester Medical Centre (URMC) in New York, showed that infants born premature lack alveolar type II cells – responsible for producing pulmonary surfactant, a vital compound for the developing lungs – as opposed to healthy infants who have these cells in abundance.
As the lungs mature after birth, some of these cells may get pruned away.
But, the lungs of premature infants take this process too far, pruning too many of the type II cells, which increases their risk of vulnerability to influenza and other lung diseases.
In the study published in the American Journal of Respiratory Cell and Molecular Biology, when newborn mice were exposed to extra oxygen at birth – which caused their lungs to respond and develop similarly to those of preterm infants – they ended up with far fewer of these cells once they reached adulthood.
Due to the absence of the type II cells, these mice responded worse when exposed to influenza virus as adults, and developed a much more severe disease than mice born in a traditional oxygen environment.
The discovery may provide a potential explanation for preterm infants' added susceptibility to influenza and other lung diseases later in their lives, the researchers said.
"There's a direct correlation between the loss of these cells and an inferior response to lung disease, and we do know that there's something about that early oxygen-rich environment that causes a mouse to respond poorly to viral infection later in life," O'Reilly from the URMC said.