title: Activation of circulating polymorphonuclear leukocytes in preterm infants with severe idiopathic respiratory distress syndrome.
abstract: 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.
authors.affiliation: Beatrix Childrens Hospital, Division of Neonatology, University Hospital Groningen, The Netherlands.
authors.forename: F
authors.initials: F
authors.lastname: Brus
authors.forename: W
authors.initials: W
authors.lastname: van Oeveren
authors.forename: A
authors.initials: A
authors.lastname: Okken
authors.forename: S O
authors.initials: SO
authors.lastname: Bambang
mesh_terms: D015926:Complement C3a / Q000031:analogs & derivatives / Q000276:immunology; D005260:Female; D006801:Humans; D007231:Infant, Newborn; D007958:Leukocyte Count; D019272:Leukocyte Elastase / Q000276:immunology; D008213:Lymphocyte Activation / Q000276:immunology*; D008297:Male; D009504:Neutrophils / Q000276:immunology*; D007752:Obstetric Labor, Premature; D010972:Platelet Activating Factor / Q000276:immunology; D011247:Pregnancy; D012127:Respiratory Distress Syndrome, Newborn / Q000276:immunology*; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology; D012122:Ventilators, Mechanical; D000515:alpha 1-Antitrypsin / Q000276:immunology
chemical_list: D010972:Platelet Activating Factor; D014409:Tumor Necrosis Factor-alpha; D000515:alpha 1-Antitrypsin; C037741:alpha 1-antitrypsin-leukocyte elastase complex; C044541:complement C3a, des-Arg-(77)-; D015926:Complement C3a; D019272:Leukocyte Elastase