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Am J Physiol Lung Cell Mol Physiol 285: L121-L129, 2003. First published February 28, 2003; doi:10.1152/ajplung.00393.2002
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Minimal lung and systemic responses to TNF-{alpha} in preterm sheep

Machiko Ikegami,1 Timothy J. M. Moss,2 Suhas G. Kallapur,1 Neil Mulrooney,1 Boris W. Kramer,1 Ilias Nitsos,2 Cindy J. Bachurski,1 John P. Newnham,2 and Alan H. Jobe1

1Cincinnati Children's Hospital Medical Center, Division of Pulmonary Biology, Cincinnati, Ohio 45229; and 2School of Women's and Infants' Health, The University of Western Australia, Perth, 6009 Australia

Submitted 18 November 2002 ; accepted in final form 24 February 2003

TNF-{alpha} has been associated with chorioamnionitis and the subsequent development of bronchopulmonary dysplasia in preterm infants. We asked whether bioactive recombinant ovine TNF-{alpha} could induce chorioamnionitis, lung inflammation, lung maturation, and systemic effects in fetal sheep. We compared the responses to IL-1{alpha}, a cytokine known to induce these responses in preterm sheep. Intra-amniotic TNF-{alpha} caused no chorioamnionitis, no lung maturation, and a very small increase in inflammatory cells in the fetal lung after 5 h, 2 days (d), and 7 d. In contrast, IL-1{alpha} induced inflammation and lung maturation. TNF-{alpha} given into the airways at birth increased granulocytes in the bronchoalveolar lavage fluid of ventilated preterm lungs and decreased the mRNA for surfactant protein C but did not adversely effect postnatal lung function. An intravascular injection of IL-1{alpha} caused a systemic inflammatory response in fetal sheep, whereas there was no fetal response to intravascular TNF-{alpha}. Fetal and newborn preterm sheep are minimally responsive to TNF-{alpha}. Therefore, the presence of a mediator such as TNF-{alpha} in a developing animal does not necessarily mean that it is causing the responses anticipated from previous results in adult animals.

inflammation; fetal maturation; cytokines; interleukin-1{alpha}; chorioamnionitis; endotoxin


Address for reprint requests and other correspondence: M. Ikegami, Cincinnati Children's Hospital Medical Center, Div. of Pulmonary Biology, 3333 Burnet Ave., Cincinnati, OH 45229-3039 (E-mail: machiko.ikegami{at}cchmc.org).




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