失控性炎症是启动、放大、维持急性肺损伤（ALI）/急性呼吸窘迫综合征（ARDS）的中心环节。本项目在我们前期研究发现IL-27在ARDS中上调表达、LPS可以促进AT-II细胞中IL-27R（WSX-1）上调表达的基础上，鉴于AT-Ⅱ细胞是ALI/ARDS的重要效应细胞，推测"IL-27通过结合IL-27R，进而诱导AT-II细胞产生一系列炎症因子，在ALI中推动失控性炎症，IL-27的这一促炎效应可能与PI3K/Akt的激活有关"的假说。拟于肺损伤人AT-II细胞和大鼠肺损伤模型中，通过siRNA干扰、单克隆抗体抑制、基因芯片筛选、抑制剂，结合Western Blot、ELISA、Realtime-PCR等方法，研究IL-27在ALI炎症中的作用，并初步探讨IL-27调控PI3K/Akt信号通路在ALI中作用的分子机制，将为ALI/ARDS发病机制的阐明提供理论依据，并开拓其防治新思路。

Uncontrolled inflammation is a central link to start, amplify and maintain acute lung injury(ALI)/acute respiratory distress syndrome(ARDS). Based on our previous studies which we have found the expression of IL-27 was up-regulated in ARDS and lipopolysaccharide (LPS) could promote the up-regulated expression of IL-27R(WSX-1) in AT-II cells, since AT-II cells are one of important target cells of ALI/ARDS, we provide the hypothesis that after combining with IL-27R, IL-27 could induce AT-II cells to produce a series of cytokines and then promote inflammation to be out of control in ALI, which is probable related to PI3K/Akt pathway. Our objective is to establish the ALI models in vitro and in vivo , and investigate the effect of IL-27 on ALI,Furthermore, to explore the possible mechanisms of PI3K/Akt pathway regulated by IL-27 on ALI by means of siRNA interference, inhibition of monoclonal antibodies , gene chips screening, Western Blot, ELISA, Realtime-PCR and so on, which would help to clarify the pathogenesis of ALI/ARDS and provide a new idea for prevention and therapy of ALI/ARDS.