抽象的
现在认识到,上皮细胞衬里呼吸道和肺泡能够释放各种介质,其具有调节局部炎症反应的可能性。通过在13个对照受试者的无浓性支气管血液灌洗液(BALF)和患者中,通过敏感的免疫测定,测量16kDA克拉拉细胞蛋白(CC16)的磷脂酶A2活性的抑制剂的量,通过敏感的支气管血液灌洗液(BALF)和患者急性肺损伤(14个具有全吹呼吸窘迫综合征(ARDS); 21后标准心肺旁路手术,ARDS的已知风险因素)。将CC16水平与炎症的其他标志物进行比较,具有各种分子量:白蛋白(Nephelometry);总蛋白质(分光光度法);β2-微球蛋白(乳胶免疫测定);胱抑素C(乳胶免疫测定);α1-抗真菌素(免疫辐射体)和Limocortin-1(酶联免疫吸附测定(ELISA))。在所有BALF中可检测到克拉拉细胞蛋白(CC16),并且在急性肺损伤患者的患者中观察到患有急性肺损伤的BALF的显着较高水平。BALF克拉克拉细胞蛋白水平的变化与α2-大粒蛋白和天然磷脂酶抑制剂Limocoratin-1不同。 Alpha 2-macroglobulin levels were not significantly enhanced in patients at risk for ARDS, but were increased in patients with ARDS; whereas, lipocortin 1 levels were not elevated in either group. Pretreatment of patients at risk for ARDS with high dose methylprednisolone did not alter the amount of Clara cell protein recovered in BALF. The mean CC16 level in BALF from patients with ARDS who died was significantly lower than from those who survived. The data presented in this study suggest that pulmonary epithelial cells secrete a natural anti-inflammatory protein during acute lung injury, which might have a protective and immunosuppressive role.