INTERLEUKIN-1-BETA-INDUCED NEUTROPHIL RECRUITMENT AND ACUTE LUNG INJURY IN HAMSTERS
INTERLEUKIN-1-BETA-INDUCED NEUTROPHIL RECRUITMENT AND ACUTE LUNG INJURY IN HAMSTERS
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DOI：
10.1007/bf01534377
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发表时间：
1995-02-01
期刊：
影响因子：
5.1
通讯作者：
REPINE, JE
中科院分区：
文献类型：
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作者：
PATTON, LM;SAGGART, BS;REPINE, JE
重组白介素1β(IL-1β)气管内注射可引起金黄地鼠肺内中性粒细胞聚集和肺损伤。气管内注射IL-1β25、50或100 ng的仓鼠肺灌洗液中中性粒细胞的百分比逐渐增加。肺损伤，反映为肺灌洗液蛋白浓度和肺灌洗液血红蛋白浓度的增加，在给予100 ng IL-1β后2小时增加。肺损伤，以肺湿重/体重比率反映，遵循类似的模式，显著增加发生在注射50或100 ng IL-1后2小时。我们的结果表明，肺内IL-1β浓度的增加可导致中性粒细胞募集和肺损伤。这一机制可能有助于肺中性粒细胞聚集和肺损伤的发展，这是呼吸道IL-1β水平升高的ARDS患者的特征。
Administering recombinant interleukin-1 beta (IL-1 beta) intratracheally caused lung neutrophil accumulation and lung injury in hamsters. The percentage of leukocytes that were neutrophils increased progressively in lavages from lungs of hamsters given 25, 50, or 100 ng IL-1 beta intratracheally 2 h before. Lung injury, reflected by increased lung lavage protein concentrations and lung lavage hemoglobin concentrations, increased 2 h after administering 100 ng IL-1 beta. Lung injury, reflected by lung wet weight/body weight ratios, followed similar patterns, with significant increases occurring 2 h after insufflating 50 or 100 ng IL-1. Our results indicate that increased concentrations of IL-1 beta in lung airways can cause neutrophil recruitment and lung injury in hamsters. This mechanism may contribute to the development of lung neutrophil accumulation and lung injury that characterizes ARDS patients who have increased airway levels of IL-1 beta.