期刊
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
卷 282, 期 3, 页码 L411-L420出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajplung.00097.2001
关键词
respiratory distress syndrome; bronchopulmonary dysplasia; chorioamnionitis; surfactant; cytokines
资金
- NHLBI NIH HHS [HL-65397] Funding Source: Medline
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL065397] Funding Source: NIH RePORTER
Antenatal inflammation may be an important triggering event in the pathogenesis of bronchopulmonary dysplasia but may also accelerate fetal lung maturation. We examined the effects of intra-amniotic (IA) interleukin (IL)-1alpha and IL-1beta on maturation of the fetal sheep lung. These cytokine effects were compared with IA endotoxin, a potent proinflammatory stimulus that accelerated lung maturation. Date-bred ewes received 15 or 150 mug recombinant ovine IL-1alpha or IL-1beta or 10 mg Escherichia coli endotoxin by IA injection at 118 days gestation (term = 150 days), and fetuses were delivered at 125 days. IL-1alpha and IL-1beta improved lung function and increased alveolar saturated phosphatidylcholine (Sat PC) and surfactant protein mRNA expression at the higher dose. The maturation response to IL-1alpha was greater than that to IL-1beta, which was similar to endotoxin response. Inflammation was also more pronounced after IL-1alpha treatment. Only endotoxin animals had residual inflammation of the fetal membranes at 7 days. Lung compliance, lung volume, and alveolar Sat PC were positively correlated with residual alveolar wash leukocyte numbers 7 days after IL-1 treatment, suggesting a link between lung inflammation and maturation.
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