Infants born preterm may lack key lung cells later in life
University of Rochester Medical Center Jun 14, 2017
Mice born into an oxygen–rich environment respond worse to the flu once fully grown due to an absence of certain lung cells, a discovery that provides a potential explanation for preterm infants added susceptibility to influenza and other lung diseases later in their lives, according to new research from the University of Rochester Medical Center (URMC).
The research, published in the April issue of the American Journal of Respiratory Cell and Molecular Biology, focuses on alveolar type II cells, which help to rebuild lung tissue after damage. When newborn mice are exposed to extra oxygen at birth – which causes their lungs to respond and develop similarly to those of preterm infants – they end up with far fewer of these cells once they reach adulthood.
Once exposed to influenza virus as adults, these mice then developed a much more severe disease than mice born in a traditional oxygen environment.
ÂWe donÂt know if this is exactly what happens in preterm infants, said Michael OÂReilly, PhD, Professor of Pediatrics, Environmental Medicine, and Oncology at URMC. ÂBut we do know that thereÂs a direct correlation between the loss of these cells and an inferior response to lung disease, and we do know that thereÂs something about that early oxygen–rich environment that causes a mouse to respond poorly to viral infection later in life. So this helps connect those dots.Â
OÂReilly, who studies the developmental origins of lung disease, hopes to now pursue research on the life cycle of alveolar type II cells. The cells are abundant in the lungs of healthy infants, as they are responsible for producing pulmonary surfactant, a vital compound for the developing lung. As the lungs mature after birth, some of these cells may be pruned away. In theory, the lungs of premature infants take this process too far, pruning too many type II cells.
ÂRight now, we donÂt really understand the biology of that, said OÂReilly. ÂBut once we do, that opens the door to exploring a potential treatment.Â
Min Yee, technical associate in OÂReillyÂs research group, was the articleÂs lead author. In addition to OÂReilly, William Domm, PhD, Robert Gelein, Karen Bentley, Matthew Kottman, MD, Paige Lawrence, PhD, Patricia Sime, MD, were co–authors on the study.
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The research, published in the April issue of the American Journal of Respiratory Cell and Molecular Biology, focuses on alveolar type II cells, which help to rebuild lung tissue after damage. When newborn mice are exposed to extra oxygen at birth – which causes their lungs to respond and develop similarly to those of preterm infants – they end up with far fewer of these cells once they reach adulthood.
Once exposed to influenza virus as adults, these mice then developed a much more severe disease than mice born in a traditional oxygen environment.
ÂWe donÂt know if this is exactly what happens in preterm infants, said Michael OÂReilly, PhD, Professor of Pediatrics, Environmental Medicine, and Oncology at URMC. ÂBut we do know that thereÂs a direct correlation between the loss of these cells and an inferior response to lung disease, and we do know that thereÂs something about that early oxygen–rich environment that causes a mouse to respond poorly to viral infection later in life. So this helps connect those dots.Â
OÂReilly, who studies the developmental origins of lung disease, hopes to now pursue research on the life cycle of alveolar type II cells. The cells are abundant in the lungs of healthy infants, as they are responsible for producing pulmonary surfactant, a vital compound for the developing lung. As the lungs mature after birth, some of these cells may be pruned away. In theory, the lungs of premature infants take this process too far, pruning too many type II cells.
ÂRight now, we donÂt really understand the biology of that, said OÂReilly. ÂBut once we do, that opens the door to exploring a potential treatment.Â
Min Yee, technical associate in OÂReillyÂs research group, was the articleÂs lead author. In addition to OÂReilly, William Domm, PhD, Robert Gelein, Karen Bentley, Matthew Kottman, MD, Paige Lawrence, PhD, Patricia Sime, MD, were co–authors on the study.
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