IL-1α causes lung inflammation and maturation by direct effects on preterm fetal lamb lungs

Ilene R.S. Sosenko, Suhas G. Kallapur, Ilias Nitsos, Timothy J.M. Moss, John P. Newnham, MacHiko Ikegami, Alan H. Jobe

Research output: Contribution to journalArticlepeer-review

29 Scopus citations


Intra-amniotic endotoxin induces IL-1, causes chorioamnionitis, lung inflammation, lung injury and lung maturation in preterm lambs. Intra-amniotic IL-1α also causes chorioamnionitis, lung inflammation and lung maturation. We asked if IL-1α effects on the preterm lung are mediated by direct signaling to the lung rather than by indirect effects from the chorioamnionitis. To study IL-1 effects independently of chorioamnionitis, the lungs and the amniotic fluid were surgically separated in fetal sheep by diverting fetal lung fluid via a tracheostomy tube to a sialastic bag. A mini-osmotic pump delivered an intratracheal infusion of recombinant sheep IL-1α (10 μg) or saline (control) over 24 h. Preterm lambs were delivered 1d or 7d after the start of the infusion at 124d gestational age (Term = 150d). IL-1α recruited inflammatory cells and increased pro-inflammatory cytokine mRNA expression in the fetal lungs. Compared with controls, IL-1α did not alter lung antioxidant enzyme activity or alveolar numbers. IL-1α had minimal effects on the mRNA or protein expression of proteins essential for vascular development. IL-1α induced large increases in alveolar surfactant saturated phosphatidylcholine and increased lung gas volumes. Lung inflammation and maturation result from direct exposure of the fetal lung to a single cytokine - IL-1α.

Original languageEnglish (US)
Pages (from-to)294-298
Number of pages5
JournalPediatric Research
Issue number3
StatePublished - Sep 2006
Externally publishedYes

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health


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