Amniotic fluid concentrations of proinflammatory cytokines, particularly IL-1, are increased in preterm labor occuring in the setting of intraamniotic infection. Infants prenatally exposed to chorioamnionitis are less likely to have respiratory distress syndrome than newborns not exposed to intrauterine infection (Pediatrics 97:210, 1996). However, after birth, high levels of IL-1 in airway specimens are associated with surfactant dysfunction, with chronic lung disease, and with adult respiratory distress syndrome. Intraamniotic of IL-1α (150-1500 ng) promotes maturation of the fetal lung by enhancing the expression of surfactant proteins SP-A and SP-B and by improving dynamic compliance of the lungs without decreasing growth of the fetus or the lung (J Clin Invest 99:2992, 1997). We hypothesized that the effects of IL-1 are dependent on the degree of maturity.

Methods: Lung explants from fetal (19 to 30 days), 1-day newborn and adult rabbits were cultured in the presence of IL-1α (57 to 570 ng/ml) or tumor necrosis factor (TNF, 10-100 ng/ml) for 2 to 20 h. The expression of surfactant protein mRNAs (SP-A, SP-B, and SP-C) was studied.

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