Bombesin-, calcitonin-, and serotonin-immunoreactive pulmonary neuroendocrine cells in acute and chronic neonatal lung disease.

Bombesin-, calcitonin-, and serotonin-immunoreactive pulmonary neuroendocrine cells (PNEC) were quantitated in the lungs of infants dying of hyaline membrane disease (HMD) and bronchopulmonary dysplasia (BPD). When compared with the lungs of age-matched control infants dying of noncardiopulmonary causes, infants who had HMD demonstrated a decrease in the numbers of bombesin-, calcitonin-, and serotonin-immunoreactive PNECs, while infants who had BPD demonstrated an increase. This difference was most pronounced at 2 months of age, when infants with BPD had a threefold increase in bombesin-, a tenfold increase in calcitonin-, and a 34-fold increase in serotonin-immunoreactive cells. In both control infants and infants who had acute and chronic lung disease, a consistent relationship was found between numbers of the three cell types: bombesin greater than calcitonin greater than serotonin. Radioimmunoassay of lung tissue from infants dying of HMD and BPD confirmed low levels of bombesin immunoreactivity in HMD and increased levels in BPD. Circulating plasma bombesin levels in neonates, as measured by radioimmunoassay, were significantly higher than levels found in adults. Though these findings are intriguing, the documentation of a causal relationship between observed alterations in PNEC and the vascular and gas exchange abnormalities known to be associated with HMD and BPD must await further studies.