Injury, inflammation, and remodeling in fetal sheep lung after intra-amniotic endotoxin
Injury, inflammation, and remodeling in fetal sheep lung after intra-amniotic endotoxin
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DOI：
10.1152/ajplung.00407.2001
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发表时间：
2002-08-01
影响因子：
4.9
通讯作者：
Jobe, AH
中科院分区：
文献类型：
--
作者：
Kramer, BW;Kramer, S;Jobe, AH
绒毛膜炎在早产中很常见，并增加了支气管肺发育不良的风险。我们假设羊膜内毒素在子宫内损伤肺，引起一系列炎症和组织损伤，类似于在损伤的成人肺中发生的。在羊膜内注射4 mg内毒素后5 h、24 h、72 h和7 d，评价胎龄125天的早产羔羊肺的炎症、损伤和修复指标。5 h时，大气道上皮细胞表达热休克蛋白70，肺泡白细胞介素8升高。肺泡II型细胞表面活性蛋白B（SP-B）在5 h时减少，肺组织和肺泡灌洗液中SP-B在72 h时增加。到24小时，中性粒细胞被招募到大气道中，细胞死亡率最高。肺泡II型细胞在24小时减少了25%，在72小时增殖最高，与组织重塑一致。羊膜腔内内毒素引起表面活性物质分泌、炎症、细胞死亡和肺重塑，作为肺损伤的指征。恢复期伴随着胎肺的成熟变化。
Chorioamnionitis is frequent in preterm labor and increases the risk of bronchopulmonary dysplasia. We hypothesized that intra-amniotic endotoxin injures the lung in utero, causing a sequence of inflammation and tissue injury similar to that which occurs in the injured adult lung. Preterm lamb lungs at 125 days gestational age were evaluated for indicators of inflammation, injury, and repair 5 h, 24 h, 72 h, and 7 days after 4 mg of intra-amniotic endotoxin injection. At 5 h, the epithelial cells in large airways expressed heat shock protein 70, and alveolar interleukin-8 was increased. Surfactant protein B (SP-B) decreased in alveolar type II cells at 5 h, and SP-B in lung tissue and alveolar lavage fluid increased by 72 h. By 24 h, neutrophils were recruited into the large airways, and cell death was the highest. Alveolar type II cells decreased by 25% at 24 h, and proliferation was highest at 72 h, consistent with tissue remodeling. Intraamniotic endotoxin caused surfactant secretion, inflammation, cell death, and remodeling as indications of lung injury. The recovery phase was accompanied by maturational changes in the fetal lung.