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1 Division of Clinical Sciences, Center for Child Health Research, 2 University Department of Obstetrics and Gynecology, University of Western Australia, Perth, Australia; and 3 Division of Pulmonary Biology, Children's Hospital Medical Center, Cincinnati, Ohio, 45229
Antenatal
inflammation may be an important triggering event in the pathogenesis
of bronchopulmonary dysplasia but may also accelerate fetal lung
maturation. We examined the effects of intra-amniotic (IA) interleukin
(IL)-1
and IL-1
on maturation of the fetal sheep lung. These
cytokine effects were compared with IA endotoxin, a potent
proinflammatory stimulus that accelerated lung maturation. Date-bred
ewes received 15 or 150 µg recombinant ovine IL-1 or IL-1 or 10 mg Escherichia coli endotoxin by IA injection at 118 days
gestation (term = 150 days), and fetuses were delivered at 125 days. IL-1 and IL-1 improved lung function and increased alveolar
saturated phosphatidylcholine (Sat PC) and surfactant protein mRNA
expression at the higher dose. The maturation response to IL-1 was
greater than that to IL-1, which was similar to endotoxin response.
Inflammation was also more pronounced after IL-1 treatment. Only
endotoxin animals had residual inflammation of the fetal membranes at 7 days. Lung compliance, lung volume, and alveolar Sat PC were positively
correlated with residual alveolar wash leukocyte numbers 7 days after
IL-1 treatment, suggesting a link between lung inflammation and maturation.
respiratory distress syndrome; bronchopulmonary dysplasia; chorioamnionitis; surfactant; cytokines
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