Dexamethasone in vivo raises surfactant protein B mRNA in alveolar and bronchiolar epithelium

Glucocorticoids enhance the rate of maturation of the fetal lung, in part, by increasing production of surfactant by type II cells. We have examined the effect of in vivo dexamethasone treatment on mRNA levels for the hydrophobic surfactant protein, SP-B, in rat lung and compared the data to similar measurements of SP-A mRNA. Rats of known gestational and postnatal ages were injected intraperitoneally with dexamethasone (2 mg/kg) and killed after 24 h. SP-B mRNA levels in the lungs were determined by RNA blotting using rat SP-A and SP-B cDNA probes. SP-B mRNA levels increased 5.2-fold when 163 pairs of animals of all ages were examined. SP-B mRNA increases in fetuses (107 pairs) and postnatal animals (56 pairs) were 8.4- and 2.1-fold, respectively (P < 0.0001). The high levels of stimulation in fetal lungs were largely due to high increases on gestational days 18 and 19 when the control levels are very low. There were no detectable gender differences in the population as a whole. Tissue in situ hybridization showed that type II cells, as well as some bronchiolar cells, responded to dexamethasone treatment throughout life. The significance and the reasons for the presence and hormonal responsiveness of SP-B in the bronchiolar epithelium are intriguing and warrant further investigation.