Bronchopulmonary dysplasia (BPD; O2 requirement at 36 wks post conceptional age) is a common multifactorial respiratory disorder involving volutrauma followed by a pathological inflammatory response associated with increased IL-8, IL-6 and elevated tracheal aspirate neutrophils (TAN; Munshi et al, Peds Pulm.24:331,1997). Since rhG-CSF significantly increases the ANC(absolute neutrophil count), it may affect TAN as well as IL-8 tracheal levels(IL-8 positive/negative predictive value ≈70-80%) and the risk for BPD. Over a 36 month period (1994-1997), we followed 70 ventilated premature infants with birth weights <1000g and divided them into 2 groups: Septic(n=30) and non-septic (n=40). The incidence of BPD was highest in lower gestational age neonates (< 27wk, p<0.009), in SGA and in septic patients. rhG-CSF treatment was also associated with increased BPD but these patients were often SGA or septic as well. To help distinguish between the effect of rhG-CSF and other disease mechanisms, markers for lung inflammation were examined. We found that rhG-CSF treatment did not affect tracheal IL-8 levels in non-BPD babies (n=3; range 89-350 ng/ml day 5-7 postnatal age; normal ≤ 400 ng/ml) but were >400 ng/ml when BPD occurred (n=2; 850& 1150 ng/ml). TAN Counts for babies who developed BPD and received rhG-CSF were 14×104 cells/mm3 (n=6; independent of a 5-7 fold increase in the peripheral ANC) compared to 28×104 cells/mm3 (n=9) in those who did not receive study drug. These preliminary observations suggest that rhG-CSF treatment improves peripheral neutrophil counts without affecting TAN consistent with a “two compartment model”. Table

Table 1 No caption available.