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Articles in PresS, published online ahead of print March 22, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00407.2001
Submitted on October 19, 2001
Accepted on March 14, 2002
1 Division of Pulmonary Biology, Children's Hospital Medical Center, Cincinnati, OH, USA
* To whom correspondence should be addressed. E-mail: jobea0{at}chmcc.org.
Chorioamnionitis is frequent in preterm labor and increases the risk of bronchopulmonary dysplasia. We hypothesized that intra-amniotic endotoxin injures the lung in utero causing a sequence of inflammation and tissue injury similar to that which occurs in the injured adult lung. Preterm lamb lungs at 125d gestational age were evaluated for indicators of inflammation, injury and repair 5h, 24h, 72h and 7d after 4mg intra-amniotic endotoxin injection. At 5h the epithelial cells in large airways expressed heat shock protein 70 and alveolar IL-8 was increased. Surfactant protein B (SP-B) decreased in alveolar type II cells at 5h, and SP-B in lung tissue and alveolar lavage fluid increased by 72h. By 24h neutrophils were recruited into the large airways and cell death was the highest. Alveolar type II cells decreased by 25% at 24h, and proliferation was highest at 72h, consistent with tissue remodeling. Intra-amniotic endotoxin caused surfactant secretion, inflammation, cell death and remodeling as indications of lung injury. The recovery phase was accompanied by maturational changes in the fetal lung.
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