Ballabh Praveen, Simm M, Kumari J, Califano C, Aghai Z, Laborada G, Sison C, Cunningham-Rundles S
Division of Neonatology, New York Presbyterian Hospital-Weill Medical College of Cornell University, New York, New York, USA.
Pediatr Pulmonol. 2003 May;35(5):392-9. doi: 10.1002/ppul.10279.
The first objective of this study was to evaluate longitudinal changes in respiratory burst activity in circulating neutrophils and monocytes in infants of less than 30 weeks of gestation with respiratory distress syndrome (RDS), and to examine differences in neonates who subsequently developed bronchopulmonary dysplasia (BPD) compared with those neonates who did not. The second objective was to investigate the effects of dexamethasone on respiratory burst activity in neutrophils and monocytes. We measured burst activity on neutrophils and monocytes in fresh heparinized blood in response to E. coli, N-formyl-met-leu-phe (fMLP), and phorbol 12-myristate 13-acetate stimulation on days 3, 7, 14, and 21 of life, before and 2-3 days after initiating a 6-day course of dexamethasone treatment. Infants with RDS participating in the study were followed until discharge, and were classified as non-BPD and either 1) BPD d28, reflecting their oxygen requirement at day of life 28, or 2) BPD 36 weeks, reflecting oxygen dependence at 36 weeks' corrected gestational age. The diagnosis of BPD was supported by radiological changes of BPD. The percentage of activated neutrophils producing a respiratory burst increased in all premature infants with increasing postnatal days during the first 28 days of life, when the physiological stimulus E. coli was used as an activator (P < 0.02). There was no significant difference in respiratory burst activity measured either as percent activation or as mean fluorescence intensity between non-BPD and BPD infants after adjusting for the difference in weight and gestational age between the two groups. The treatment of premature infants with dexamethasone was associated with decreased activation of neutrophils (P < 0.005) when E. coli was used as a stimulus. In conclusion, a significant increase in neutrophil respiratory burst activity occurs during the first month of life in very low birth weight infants. Greater pulmonary damage in BPD cannot be attributed to reduced burst activity in either neutrophils or monocytes. Dexamethasone treatment was associated with decreased neutrophil respiratory burst activity.
本研究的首要目标是评估胎龄小于30周且患有呼吸窘迫综合征(RDS)的婴儿循环中性粒细胞和单核细胞中呼吸爆发活性的纵向变化,并检查随后发生支气管肺发育不良(BPD)的新生儿与未发生BPD的新生儿之间的差异。第二个目标是研究地塞米松对中性粒细胞和单核细胞呼吸爆发活性的影响。我们在出生后第3天、第7天、第14天和第21天,以及在开始为期6天的地塞米松治疗前和治疗后2 - 3天,测量新鲜肝素化血液中中性粒细胞和单核细胞对大肠杆菌、N - 甲酰 - 甲硫氨酰 - 亮氨酰 - 苯丙氨酸(fMLP)和佛波酯12 - 肉豆蔻酸酯13 - 乙酸酯刺激的爆发活性。参与研究的患有RDS的婴儿随访至出院,并分为非BPD组以及以下两类BPD组:1)BPD d28,反映出生后第28天的氧需求;2)BPD 36周,反映矫正胎龄36周时的氧依赖情况。BPD的诊断由BPD的影像学改变支持。当使用生理刺激物大肠杆菌作为激活剂时,在出生后的前28天内,所有早产婴儿中产生呼吸爆发的活化中性粒细胞百分比随出生后天数增加而升高(P < 0.02)。在调整两组体重和胎龄差异后,非BPD组和BPD组婴儿在以活化百分比或平均荧光强度衡量的呼吸爆发活性方面无显著差异。当地塞米松以大肠杆菌作为刺激物时,对早产婴儿的治疗与中性粒细胞活化降低相关(P < 0.005)。总之,极低出生体重婴儿在出生后的第一个月中性粒细胞呼吸爆发活性显著增加。BPD中更严重的肺损伤不能归因于中性粒细胞或单核细胞爆发活性降低。地塞米松治疗与中性粒细胞呼吸爆发活性降低相关。