Abstract
Fetal lung maturation, especially the onset of surfactant formation by alveolar type II cells, seems to be regulated by endogenous fetal glucocorticoids1–3. Recent studies4,5 suggest that glucocorticoids do not act directly on the type II cell but rather on the lung mesenchyme. In response to glucocorticoids, the mesenchyme produces and secretes a polypeptide, fibroblast–pneumonocyte factor, which in turn stimulates surfactant synthesis by the alveolar type II cell6. We report here the generation of hybridomas secreting monoclonal antibodies to rat lung fibroblast–pneumonocyte factor. Two monoclonal antibodies studied in detail reduced the cortisol-stimulated synthesis of saturated phosphatidylcholine in organotypic cultures of fetal rat lung cells and blocked the stimulatory effect of fibroblast-pneumonocyte factor in type II cells from these cultures. When embryonic chicks were injected on day 15 of incubation with either monoclonal antibody, they showed on days 20 and 21 biochemical evidence of delayed lung maturation as compared with controls. These effects were organospecific. Our observations support a physiological role for fibroblast–pneumonocyte factor in prenatal lung maturation.
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Post, M., Floros, J. & Smith, B. Inhibition of lung maturation by monoclonal antibodies against fibroblast–pneumonocyte factor. Nature 308, 284–286 (1984). https://doi.org/10.1038/308284a0
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DOI: https://doi.org/10.1038/308284a0
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