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Articles in PresS, published online ahead of print December 6, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00344.2002
Submitted on October 15, 2002
Accepted on December 2, 2002
1 Division of Pulmonary Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA
2 The University of Western Australia, School of Women's and Infant's Health, Perth, WA, Australia
* To whom correspondence should be addressed. E-mail: suhas.kallapur{at}chmcc.org.
Antenatal betamethasone is widely used in women with asymptomatic chorio-amnionitis at risk for preterm delivery but its effects on fetal inflammation are unstudied. Groups of ewes at 109±1d gestation received the following treatments: intra-amniotic (IA) saline (Control); 0.5mg/kg intra-muscular betamethasone (Beta); IA 10mg endotoxin (Endo); Beta + 2h later Endo (Beta+Endo). Beta suppressed Endo induced lung inflammation at 1d. However, compared with Endo 5d after treatment, Beta+Endo lambs had increased alveolar neutrophils, pro-inflammatory cytokine mRNA expression and serum amyloid A3 (SAA3) mRNA expression. IL-1
mRNA expression was localized to the inflammatory cells while SAA3 mRNA expression was induced in the bronchial epithelium and the inflammatory cells. Compared with Endo, Beta+Endo lambs had increased lung inflammation but equivalent lung volumes 15d after treatment. The late increase in inflammation in the Beta+Endo animals suggests that glucocorticoids impair the ability of preterm lung to down regulate endotoxin induced inflammation after fetal clearance of the glucocorticoids. These results have implications for lung inflammation and BPD in preterm infants exposed to chorio-amnionitis and maternal glucocorticoids.
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