PTGES2是一个广泛表达于脑、心脏、骨骼肌、肾和肝等多个组织中的转录因子，但其生物学功能目前尚不清楚。申请者在首次发现PTGES2具有促炎功能的基础上，进一步研究发现在炎症反应中PTGES2对自噬具有调控作用。自噬是炎症反应的重要调控因素之一，因此，本项目提出"PTGES2通过调控自噬而促进LPS 所致的炎症反应"的工作假说。本项目拟在此基础上，深入探讨PTGES2在LPS所致炎症反应中的表达模式；采用PTGES基因过表达及RNA干扰从正反两方面探讨PTGES2对LPS所致炎性小体活化及其下游炎症介质生成与释放的影响；并通过深入探讨PTGES2对自噬的调节作用从而阐明PTGES2调控炎性小体活化的机制；采用慢病毒注射的方法从整体动物水平探讨PTGES2在炎症反应中的功能。开展本项目研究，可望揭示PTGES2在LPS 所致炎症反应的调控作用及其机制，为脓毒症等炎症相关疾病的防治提供新线索。

PTGES2 is a transcription factor which is expressed in the brain, heart, skeletal muscle, kidney and liver, but its function is still not clear.In this study PTGES2 is found promoting the inflammation induced by LPS for the first time; further study indicates that PTGES2 can regulate autophagy in response to LPS stimuli. As autophagy is important in regulating inflammation, it is supposed that PTGES2 regulates LPS-induced inflammation via inhibiting autophagy. In this program we will further detect the expession of PTGES2 in LPS-induced inflammation; illustrate the pro-inflammatory function of PTGES2; and determine if PTGES2 regulates LPS-induced inflammation via regulating autophagy. In together, we expect to illustrate the function of PTGES2 and its mechanism in inflammation.