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Division of Neonatology and Pulmonary Biology, Children's Hospital Medical Center, Cincinnati, Ohio 45229-3039
Bronchopulmonary
dysplasia (BPD) commonly develops in premature infants. An improved
understanding of the pathophysiology of BPD requires better models. In
this study, neonatal FVB/N mice were exposed to room air
or 85% oxygen for 28 days. Neonatal hyperoxia resulted in decreased
alveolar septation, increased terminal air space size, and increased
lung fibrosis. These changes were evident after 7 days and more
pronounced by 28 days. Decreased alveolarization was preceded by
decreased proliferation of lung cells. After 3 days of hyperoxia, cell
proliferation was decreased compared with room air littermates. Cell
proliferation continued to be decreased in the first 2 wk but
normalized by 4 wk. Hyperoxia caused an increased number of
inflammatory cells in lung tissue and in lung lavage fluid. Analysis of
lung tissue RNA by RT-PCR showed that hyperoxia increased expression of
the proinflammatory cytokines interleukin-1
and macrophage
inflammatory protein-1. Prolonged neonatal hyperoxia caused
functional changes, decreasing lung volume and pulmonary compliance. We
conclude that prolonged exposure of neonatal mice to hyperoxia creates
a lesion that is very similar to human BPD and suggests that altered
cell proliferation may be important in the pathogenesis of chronic
neonatal lung disease.
bronchopulmonary dysplasia; lung; cell proliferation; newborn
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