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Am J Physiol Lung Cell Mol Physiol 284: L633-L642, 2003. First published December 6, 2002; doi:10.1152/ajplung.00344.2002
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Vol. 284, Issue 4, L633-L642, April 2003

Maternal glucocorticoids increase endotoxin-induced lung inflammation in preterm lambs

Suhas G. Kallapur1, Boris W. Kramer1, Timothy J. M. Moss2, John P. Newnham2, Alan H. Jobe1, Machiko Ikegami1, and Cindy J. Bachurski1

1 Cincinnati Children's Hospital Medical Center, Division of Pulmonary Biology, Cincinnati, Ohio 45229-3039; and 2 School of Women's and Infants' Health, The University of Western Australia, Perth, Western Australia, 6008 Australia

Antenatal betamethasone (Beta) is widely used in women with asymptomatic chorioamnionitis at risk for preterm delivery, but its effects on fetal inflammation are unstudied. Groups of ewes at 109 ± 1 days of gestation received the following treatments: intra-amniotic (IA) saline (control), 0.5 mg/kg intramuscular Beta, 10 mg IA endotoxin (Endo), and Beta + 2 h later Endo (Beta + Endo). Beta suppressed Endo-induced lung inflammation at 1 day. However, compared with Endo 5 days after treatment, Beta + Endo lambs had increased alveolar neutrophils, proinflammatory cytokine mRNA expression, and serum amyloid A3 (SAA3) mRNA expression. IL-1beta mRNA expression was localized to the inflammatory cells, whereas 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 15 days after treatment. The late increase in inflammation in the Beta + Endo animals suggests that glucocorticoids impair the ability of the preterm lung to downregulate Endo-induced inflammation after fetal clearance of the glucocorticoids. These results have implications for lung inflammation and bronchopulmonary dysplasia in preterm infants exposed to chorioamnionitis and maternal glucocorticoids.

bronchopulmonary dysplasia; acute-phase reactant; proinflammatory cytokines; endotoxin tolerance; chorioamnionitis


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