Analysis of Surfactant-associated Proteins in injured lungs

我们研究了急性肺损伤和哮喘肺的窒息系统。我们发现，抑制蛋白A （SP-A）可以刺激支气管上皮细胞趋化，提示SP-A可能在肺损伤后的修复中发挥凝血剂的作用。我们也报道了LPS损伤大鼠肺表面活性剂系统和代谢的改变。我们还报道了慢性哮喘豚鼠模型中表面活性剂的组成和功能变化以及支气管哮喘患者气道中SP-A水平升高。研究了表面活性剂与嗜酸性粒细胞的相互作用。结果表明，表面活性剂可诱导嗜酸性粒细胞凋亡，抑制嗜酸性粒细胞产生il -8，抑制ECP脱颗粒。这些新发现为研究表面活性剂参与支气管哮喘和急性肺损伤的发病机制开辟了新的思路。

We investigated suffactant system in acute lung injury and asthmatic lungs. We found that suffactant protein A (SP-A) could stimulate chemotaxis of bronchial epithelial cells, suggesting that SP-A might play a role in lung repair following injury as a chernoattractant. We also reported that altered surfactant system and metabolism in rat lungs injured by LPS instillation. We also reported compositional and functional changes of surfactant in a guinea pig model of chronic asthma and increased levels of SP-A in the airway in patients with bronchial asthma. The interactions between surfactant and eosinophils were also studied. We demonstrated surfactant could induce apoptosis of eosinophils, surpress IL-8production by eosinophils and inhibit ECP degranulation. All these new findings must open a new array to study the involvement of surfactant in the pathogenesis of bronchial asthma and acute lung injury.