| Objectives:Although surfactant deficiency represents the main cause of neonatal respiratory distress syndrome (NRDS) in preterm infants, several observations imply that early inflammatory response involving activated neutrophils, tissue macrophages, and cytokines plays an important role in the pathogenesis of NRDS and progression to bronchopulmonary dysplasia (BPD). Neutrophils are the first type of inflammatory cells migrating into the lungs during NRDS, and are important in the repair process, but they may also cause tissue injury. Neutrophils play an important role through activating and migrating into the tissues during the early stages of NRDS. Neutrophil attachment to the vascular endothelial cell adhesion molecules is a key event in the initiation of an inflammatory response of neutrophil migration into inflamed tissue and is mediated by proteins expressed on the surface of the neutrophil and the endothelium. Members of two important families of adhesion molecules are CD11b/CD18 and soluble intercellular adhesion molecule-1 (sICAM-1). CD11b/CD18, indicators of neutrophil activation, has emerged as a critical molecule in neutrophil dependent inflammation. sICAM-1 binds to neutrophil ligands and lead to a series of adhesive interactions. However, our knowledge about the mechanism of CD11b/CD18 and sICAM-1 in the pathogenesis of NRDS is not yet fully understood. The aim of this study was to explore functions of surface expression of CD11b/CD18 on neutrophil and the concentration of sICAM-1, which is an important ligand for CD11b/CD18, in airway aspirates (AA) supernatant at the molecular level. Further understanding of the role of inflammation in the pathogenesis and pathophysiology of NRDS may lead to new prevention and/or treatment strategies. Methods : The study population consisted of fifteen preterm infants with NRDS, including seven mild NRDS and eight severe NRDS, and fifteen age-matched control patients without RDS. The patients of two groups were required intubation and mechanical ventilation. The two groups were comparable regarding perinatal characteristics. The whole samples were taken from the infants on 24h and 72h after birth. None of the neonates studied had any clinical or laboratory evidence of infection by the time of sampling. Neutrophil surface expression of CD11b/CD18 was quantified with immunofluorescence flow cytometry method. sICAM-1 was measured using a sandwich Enzyme-Linked Immunosorbent Assay (ELISA) method. Results 1.CD11b: In preterm infants with NRDS, neutrophil CD11b expression on 24h and 72h after birth [(57.857±14.977)% and (91.496 ±5.293)% , respectively] was significantly higher than that in control group.[(22.553 ±14.610)% and (23.513±16.918)%, respectively, P<0.01 and P<0.01, respectively]. The percent positive cell (PPC) of neutrophils expressing CD11b of the infants with NRDS on 72h after birth was significantly higher than that on 24h after birth. (P<0.01) And there was significant difference of neutrophil CD11b expression between mild NRDS group and severe NRDS group on 24h and 72h after birth. (P<0.01and P<0.01, respectively) 2.CD18: On 24h and 72h after birth, CD18 expression level on neutrophils of the preterm infants with NRDS[(26.940±10.902)% and (80.584 ±16.090)%, respectively] was significantly higher than that in control group. [(7.279 ±4.814)% and(7.385±4.052)%, respectively, P<0.01 and P<0.01, respectively ]. On 72h after birth, the PPC of neutrophils expressing CD18 was significantly higher in the NRDS group compared to on 24h after birth. (P<0.01) In each NRDS group, neutrophil CD18 expression in severe NRDS group was higher than in mild NRDS group. (P<0.01 and P<0.05, respectively) 3.sICAM-1: sICAM-1 level in the AA supernatant was significantly higher in the preterm infants with NRDS on 24h and 72h after birth[(88.503 ±14.536)% and (179.957 ±71.029)%, respectively] than that in control group. [(28.739±19.234)pg/ml and (31.189±20.795)pg/ml, respectively, P<0.01 and P<0.01, respectively]. The level of sICAM-1 in the preterminfants with NRDS on 7...
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