The production of the proinflammatory cytokine IL-1 is increased in the fetal compartment in cases of preterm labor associated with intrauterine infection. The production of EGF, on the other hand, increases with advancing gestation. Both IL-1 and EGF upregulate the expression of SP-A. However, IL-1 may also have deleterious effects on the developing lung, since an elevated IL-1 concentration in lung effluent is associated with the development of chronic lung disease in the newborn. IL-10 is an anti-inflammatory cytokine that inhibits the production of IL-1 and of other proinflammatory cytokines.Aim. We investigated 1) whether IL-10 affects SP-A expression in lung explants and 2) whether IL-10 modulates SP-A expression in explants treated with IL-1 or EGF. Methods. Fetal rabbit lung explants(gestational age 22 days) were treated with IL-1 (570 ng/ml), EGF (50 ng/ml) or IL-10 (5 ng/ml) for 24 or 72 hours. Expression of SP-A mRNA was quantitated by Northern blotting. Results. SP-A expression at 24 and 72 h as percent of the respective controls (±SE) was:Table Thus, IL-1 and EGF enhanced SP-A expression, but did not potentiate each other's effects. IL-10 alone had no effect on SP-A expression. IL-10 suppressed the stimulatory effect of IL-1 in explants treated for 72 h, but not in those treated for 24 h. IL-10 did not suppress SP-A expression in EGF-treated explants. Conclusion. IL-10 selectively counteracts the effect of IL-1 but not that of EGF on SP-A expression. IL-10 may be of value in inhibiting lung inflammation caused by proinflammatory cytokines. The potential of IL-10 in preventing inflammation in the lungs without affecting maturational events unrelated to inflammation, should be further investigated.

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