Activation of circulating polymorphonuclear leukocytes in preterm infants with severe idiopathic respiratory distress syndrome.

We have studied activation of circulating polymorphonuclear leukocytes (PMN) in plasma of preterm infants with severe idiopathic respiratory distress syndrome (IRDS group, n = 15) and without IRDS (reference group, n = 15) during the first 5 postnatal days. We have observed lower median PMN counts in the IRDS group than in the reference group from d 2 (1.4 x 10(9)/L versus 4.8 x 10(9)/L in the reference group, p < 0.001) to d 4 to 6 (1.6 x 10(9)/L versus 4.0 x 10(9)/L, p < 0.01). Lower PMN counts in the IRDS infants were accompanied by lower median plasma elastase-alpha1-proteinase inhibitor (PI) concentrations (53.6 ng/mL versus 128.0 ng/mL in the reference group on d 2, p < 0.05). Simultaneously, median elastase-alpha1-PI/PMN ratios of these infants were significantly higher (40.8 ng/10(6) PMN versus 21.8 ng/10(6) PMN on d 2, p < 0.05), indicating activation of circulating PMN. Activation of circulating PMN in the IRDS group is associated with platelet-activating factor (PAF) release and complement activation from within 6 to 12 h of birth but not with release of tumor necrosis factor-alpha. PAF release was represented by significantly reduced inhibiting capacity (58% of normal human plasma, p < 0.01) and complement activation by higher median plasma C3a des-Arg concentrations (1680 ng/mL versus 325 ng/mL in the reference group, p < 0.001). We conclude that circulating PMN are activated in preterm infants with severe IRDS, which might be caused by systemic PAF release and complement activation. This activation process may play a role in the pathogenesis of the IRDS by influx of activated PMN into the lungs.