Neonatal lung neutrophils and elastase/proteinase inhibitor imbalance.

Neonatal lung neutrophils and elastase/proteinase inhibitor imbalance.
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新生儿肺中性粒细胞和弹性蛋白酶/蛋白酶抑制剂失衡。

DOI:
10.1164/arrd.1984.130.5.817
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发表时间:
1984
期刊:
The American review of respiratory disease
影响因子:
--
通讯作者:
Johnson,JD
Johnson,JD
中科院分区:
--
文献类型:
--
作者:
Ogden,BE;Murphy,SA;Saunders,GC;Pathak,D;Johnson,JD

文献摘要

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对10例正常新生儿、20例呼吸窘迫综合征(RDS)和11例支气管肺发育不良(BPD)新生儿进行了前瞻性支气管肺泡灌洗(BAL),以评价肺部炎症在新生儿肺部疾病中的作用。在所有组中,在出生后< 24 h时在BAL中发现了轻微的炎症,但与对照组相比,在RDS和BPD中在96 h时观察到了显著的肺多形核白细胞(PMN)流入。出生后1周,RDS患儿BALPMN计数恢复正常,但BPD患儿BALPMN计数在5周内仍显著升高。肺泡巨噬细胞(AM)计数在RDS组96 h时显著升高(p < 0.05),而BPD组4、5 wk时显著降低(p < 0.05)。RDS患儿的BAL弹性蛋白酶/α 1蛋白酶抑制剂(α 1 Pi)比值与正常对照组无差异;然而,BPD患儿的这些比值在出生后1 - 4周显著升高,使这些婴儿处于蛋白水解性肺损伤的风险中。RDS和BPD患者灌洗液弹性蛋白酶水平均升高,与RDS患者BALα 1 Pi平行升高和BPD患者BALα 1 Pi降低相关。这些结果表明,肺部炎症,与PMN内流的延长和弹性蛋白酶和α 1 Pi之间的失衡,可能有助于新生儿慢性肺疾病,BPD的发展。
Serial bronchoalveolar lavage (BAL) was performed prospectively on 10 normal control subjects, 20 Respiratory Distress Syndrome (RDS), and 11 Bronchopulmonary Dysplasia (BPD) newborn infants to evaluate the role of pulmonary inflammation in neonatal lung disease. Minimal inflammation was found in BAL at < 24 h of life in all groups, but significant pulmonary polymorphonuclear leukocyte (PMN) influxes were noted at 96 h in RDS and BPD compared with control subjects. By 1 wk of life, BAL PMN counts returned to normal in RDS, but counts remained significantly elevated through 5 wk in BPD. Alveolar macrophage (AM) counts were significantly elevated at 96 h in RDS (p < 0.05), but were significantly depressed in BPD at 4 and 5 wk (p < 0.05). The BAL elastase/alpha1proteinase inhibitor (α1Pi) ratios in RDS did not differ from those of normal control subjects; however, these ratios were significantly elevated from 1 through 4 wk of life in BPD, placing these infants at risk for proteolytic lung damage. Lavage elastase levels were elevated in both RDS and BPD, associated with a parallel increase in BALα1Pi in RDS and depressed BALα1Pi in BPD. These findings suggest that pulmonary inflammation, associated with a prolonged PMN influx and an imbalance between elastase and α1Pi, may contribute to the development of the neonatal chronic lung disease, BPD.