Acceleration of barrier ontogenesis in vitro through air exposure.

Immaturity of the epidermal barrier in the preterm infant may have serious clinical consequences. However, regardless of the degree of prematurity, the barrier rapidly matures such that by 2 wk all infants display a competent barrier. To determine whether the change from an aqueous (intrauterine) to a xeric environment might be the stimulus for this accelerated maturation, we examined the effects of air exposure on cutaneous barrier formation in vitro. Skin explants from d 17 fetal rats were incubated either submerged or at the air-medium interface. As previously reported, a competent barrier formed under submerged conditions after 3-4 d, precisely mirroring the time course of maturation in utero. In contrast, barrier maturation was accelerated in air-exposed explants, with functional, histologic, and structural markers of barrier formation observed after only 2 d of incubation. A water-impermeable membrane blocked the acceleration of barrier formation, resulting in a developmental time course comparable to that for submerged explants. In contrast a water vapor-permeable membrane did not block the acceleration. Glucocorticoids and thyroid hormone, which accelerate barrier formation in utero or in vitro under submerged conditions, did not further accelerate barrier formation in the air-exposed model. These data indicate that: 1) air exposure accelerates barrier ontogenesis, suggesting that water flux may be an important signal for the accelerated barrier formation that occurs in premature infants; and 2) factors which accelerate barrier formation in utero may not further accelerate barrier formation in neonates.