NEONATAL LUNG NEUTROPHILS AND ELASTASE PROTEINASE-INHIBITOR IMBALANCE

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Abstract
Serial bronchoalveolar lavage (BAL) was performed prospectively on 10 normal control subjects, 20 respiratory distress syndrome (RDS), and 11 bronchopulmonary dysplasia (BPD) newborn infants to evaluate the role of pulmonary inflammation in neonatal lung disease. Minimal inflammation was found in BAL at < 24 h of life in all groups, but significant pulmonary polymorphonuclear leukocyte (PMN) influxes were noted at 96 h in RDS and BPD compared wih control subjects. By 1 wk of life, BAL PMN counts returned to normal in RDS, but counts remained significantly elevated through 5 wk in BPD. Alveolar macrophage (AM) counts were significantly elevated at 96 h in RDS (P < 0.05), but were significantly depressed in BPD at 4 and 5 wk (P < 0.05). The BAL elastase/.alpha.1-proteinase inhibitor (.alpha.1Pi) ratios in RDS did not differ from normal control subjects; However. These ratios were significantly elevated from 1-4 wk of life in BPD, placing these infants at risk for proteolytic lung damage. Lavage elastase levels were elevated in both RDS and BPD, associated with a parallel increase in BAL.alpha.1Pi in RDS and depressed BAL.alpha.1Pi in BPD. Pulmonary inflammation, associated with a prolonged PMN influx and an imbalance between elastase and .alpha.1Pi, may contribute to the development of the neonatal chronic lung disease, BPD.