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1 Division of Pulmonary Biology, Cincinnati Children's Hospital Medical Center, University of Cincinnati, College Of Medicine, Cincinnati, OH, USA
2 School of Women's and Infants' Health, The University of Western Australia, Perth, Western Australia, Australia
* To whom correspondence should be addressed. E-mail: suhas.kallapur{at}cchmc.org.
Chronic early gestational chorioamnionitis is associated with development of bronchopulmonary dysplasia in preterm infants. A single intra-amniotic exposure to endotoxin decreased alveolarization and reduced expression of endothelial proteins in 125d gestational age preterm lambs. We hypothesized that prolonged exposure to intra-amniotic endotoxin would cause progressive lung inflammation and inhibit alveolar and pulmonary vascular development. Endotoxin 1mg/d or saline was administered via an intra-amniotic osmotic pump from 80-108 days gestational age (continuous pump) or by 4 weekly 10mg intra-amniotic endotoxin injections starting at 100 days gestational age (multiple dose). Lung morphometry, lung inflammation, vascular effects and lung maturation were measured at delivery. The continuous pump lambs delivered at 100 days (approx. 70% of total endotoxin exposure) had lung inflammation, fewer saccules and decreased endothelial proteins eNOS, VEGFR2 expression compared with controls. The continuous pump (delivered at 138 days) and multiple dose lambs (delivered at 130 and 145 days) had mild persistent lung inflammation, no significant differences in lung morphometry or expression of endothelial proteins compared with controls. Surfactant saturated phosphatidylcholine pool sizes were increased in all endotoxin-exposed groups but lung function was not changed relative to controls. Contrary to our hypothesis, a prolonged fetal exposure to intra-amniotic endotoxin caused mild persistent inflammation but did not lead to progressive structural abnormalities in lungs of near-term gestation lambs.
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