DEXAMETHASONE DECREASES PULMONARY PRODUCTION OF INTERLEUKIN-8 IN VENTILATED PRETERM INFANTS AT RISK FOR BRONCHOPULMONARY DYSPLASIA

There is evidence that interleukin-8 (IL-8) is an important mediator i n the pulmonary inflammation associated with the development of bronch opulmonary dysplasia (BPD). We have recently shown that, in parallel t o reduced ventilatory support, IL-8 levels in tracheobronchial aspirat e fluid (TAF) are decreased following dexamethasone treatment. However , it is not known whether this effect is due to a decreased pulmonary production of IL-8 or due to a decreased leakage of IL-8 from plasma. To answer this question, we simultaneously determined IL-8 and albumin -levels in TAF as well as plasma levels of IL-8 in preterm infants at risk for BPD before and after dexamethasone treatment. Additionally, I L-8 levels in TAF were compared to levels of term infants ventilated f or nonpulmonary reasons (n = 8). Samples were obtained from 17 neonate s at risk for BPD (gestational age 27.4 +/- 0.6 weeks, birth weight 87 7 +/- 42 g, mean +/- SE), treatment with dexamethasone was initiated a t a median of 12 days. Following treatment with dexamethasone, TAF-lev els of IL-8 and albumin were significantly reduced (p < 0.01). Plasma levels were 200-fold lower compared with TAF values (p < 0.01), and we re not affected by dexamethasone therapy. The results demonstrate, tha t dexamethasone decreases production and/or secretion of IL-8 within t he lung. The benefit of dexamethasone in neonates with BPD may be due to a downregulation of pulmonary inflammation by a decreased local gen eration of IL-8.