急性肺损伤/急性呼吸窘迫综合症的核心病理改变是肺气血屏障的损害，其修复与内源性干细..胞增生有密切关系。外源性干细胞及上皮角化生长因子KGF-2可以减轻肺血管内皮通透性，促进肺气血屏障..的修复，改善肺损伤。但干细胞的动员、定植、增生及整合修复与所处的微环境密切相关，干细胞如何调控..免疫和炎症细胞影响微环境，微环境中哪些关键因素影响干细胞修复肺气血屏障的机制目前仍未清楚。本课..题利用转基因敲除（PAI-1，tPA，uPA，TFP1）的小鼠调控微环境凝血纤溶的变化，观察内源性干细胞，外..源性干细胞及外源性KGF-2对肺气血屏障修复的作用与机制，KGF-2促进内源性干细胞增生的机制，并采用免..疫组库的研究手段，探索上述屏障损伤与修复过程中免疫与炎症细胞表面受体的变化，阐明干细胞与微环境..相互作用的免疫机制，为临床应用干细胞和生长因子治疗肺损伤和急性呼吸窘迫综合症提供实验室的基础。

The key pathology changes of acute lung injury(ALI)/acute respiratory distress syndrome(ARDS) is blood-gas barrier damage. Exogenous stem cell and keratinocyte growth factor-2(KGF-2) could attenuate increased endothelial permeability and improve repair of pulmonary blood-gas barrier,leading to recovery of acute lung injury.However,the mobilization of stem cell, it's colonization, proliferation and integration is highly related to micro-environmental changes in the lung. It is not clear yet how stem cell modulate immunity and inflammation, and which major factors impact blood-gas barrier repair in pulmonary micro-environment. The current study is to utilize gene knockout mice(PAI-1,tPA,uPA,TFP1) as a research tool to mimic micro-environment changes, and to investigate the effects of endogenous and exogenous stem cell and KGF-2 in pulmonary blood-gas barrier repair. Immune receptor changes and interaction between immune and inflammatory cells will be studied in order to provide mechanism, and experimental envidence of cell-based therapy and growth factor based treatment in the future.