Published ahead of print on August 18, 2005, doi:10.1164/rccm.200506-1007OC
Am. J. Respir. Crit. Care Med., Volume 172, Number 10, November 2005, 1315-1321
A more recent version of this article appeared on November 15, 2005
Submitted on June 30, 2005
Accepted on August 17, 2005
Recruited Inflammatory Cells Mediate Endotoxin Induced Lung Maturation in Preterm Fetal Lambs
Suhas G Kallapur1*, Timothy J.M Moss2, Machiko Ikegami1, Richard L Jasman3, John P Newnham2, and Alan H Jobe1
1 Divison of Pulmonary Biology and Neonatology, Cincinnati Children's Hospital Medical Center, University of Cincinnati, Cincinnati, OH, USA,
2 University of Western Australia, School of Women's and Infants' Health, Perth, W. Australia, Australia,
3 ICOS Corporation, Bothell, WA, USA
* To whom correspondence should be addressed. E-mail: suhas.kallapur{at}cchmc.org.
Rationale: Chorioamnionitis is paradoxically associated with a decreased incidence of respiratory distress syndrome in preterm infants. In preterm lambs, intra-amniotic endotoxin and interleukin-1 induce lung inflammation followed by lung maturation.
Objective: To test if inflammatory cells are required to mediate induced lung maturation.
Methods: Lung inflammation was induced by intra-amniotic injection of endotoxin or IL-1. Inflammatory cell recruitment to the lung was inhibited by an anti-CD18 blocking antibody given intra-muscular to the fetus. Preterm lambs were delivered at 124d gestation (term=150d) 2 days or 7 days after exposure to endotoxin/IL-1 or endotoxin/IL-1+anti-CD18 antibody.
Measurements: Lung inflammation was measured by bronchoalveolar lavage fluid cell count, inflammatory scoring of lung parenchyma, expression of pro-inflammatory cytokines and inducible nitric oxide synthase. Lung maturation was quantitated by surfactant protein mRNA expression, saturated phosphatidyl choline pool size and pressure-volume curves.
Main results: Inhibition of CD18 significantly reduced endotoxin induced but not IL-1 induced fetal lung inflammatory cell recruitment and activation as well as expression of pro-inflammatory cytokines. Compared with controls, both endotoxin and IL-1 induced lung maturation. Anti CD18 antibody administration inhibited only endotoxin induced but not IL-1 induced increases in surfactant protein mRNA and surfactant saturated phospatidylcholine. Exposure to anti-CD18 antibody moderated endotoxin induced increases in lung volumes but had no effect on IL-1
induced increases in lung volumes.
Conclusions: i) Endotoxin but not IL-1 induced inflammatory cell recruitment in the preterm fetal lamb lung is CD18 dependent. ii) Recruited inflammatory cells mediate some aspects of fetal lung maturation.
Key words: Respiratory distress syndrome, surfactant, chorio-amnionitis, BPD, CD18
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