Phagocyte activation in preterm infants following premature rupture of the membranes or chorioamnionitis

Phagocyte activation was studied in 48 preterm infants, gestational age 27.3 +/- 0.3 wk, birthweight 968 +/- 40 g, during the first postnatal week. Human neutrophil lipocalin as a marker of neutrophil activation was measured in plasma and tracheal aspirate fractions; and lysozyme, as a marker of monocyte and macrophage activation, in plasma. The concentration of plasma human neutrophil lipocalin was 69 (46-126) mug/l (median and quartiles), tracheal aspirate fraction fluid 213 (71-133) 433) mug/l and plasma lysozyme 1337 (923-1764) mug/l. Infants born to mothers with premature rupture of the membranes or clinical chorioamnionitis (group A, n = 20) had significantly higher plasma [73 (58-151) vs 53 (38-108) mug/l; p = 0.027], and tracheal aspirate fraction human neutrophil lipocalin [319 (129-540) vs 190 (57-324) mug/l; p = 0.019], and plasma lysozyme [1739 (1356-2021) vs 1140 (739-1557) mug/l; p =0.0001] than did infants whose mothers had intact membranes and who had no suspicion of infection (Group B, n = 28). In infants born to mothers receiving corticosteroids ante partum, correlations existed between time from treatment to delivery and plasma (r = 0.322, p = 0.0256) and tracheal aspirate fraction human neutrophil lipocalin (r = 0.314, p = 0.0096). Infants born to mothers with at risk of infection are exposed to the potentially harmful effects of activated neutrophils. Premature rupture of the membranes, even without signs of clinical infection of the mother or the fetus, is associated with phagocyte activation that may begin already in utero. Corticosteroid treatment of the mother may cause transient inhibition of neutrophil activation in the newborn.