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Minimal lung and systemic responses to TNF- in preterm sheep

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- has been associated with chorioamnionitis and the subsequent development of bronchopulmonary dysplasia in preterm infants. We asked whether bioactive recombinant ovine TNF- could induce chorioamnionitis, lung inflammation, lung maturation, and systemic effects in fetal sheep. We compared the responses to IL-1, a cytokine known to induce these responses in preterm sheep. Intra-amniotic TNF- 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 induced inflammation and lung maturation. TNF- 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 caused a systemic inflammatory response in fetal sheep, whereas there was no fetal response to intravascular TNF-. Fetal and newborn preterm sheep are minimally responsive to TNF-. Therefore, the presence of a mediator such as TNF- 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; chorioamnionitis; endotoxin

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