脓毒症是重症医学领域常见的临床综合征和治疗难题。p120-catenin是新近发现的连环蛋白家族新成员，我们前期研究发现，利用siRNA沉默p120，巨噬细胞在自然状态和LPS诱导后自噬蛋白LC3-II表达均明显升高；IL-18产生显著降低，进一步研究发现，p120能与负调控蛋白mTOR相结合。为此我们提出假设：p120可能参与调控巨噬细胞自噬，进而影响脓毒症的进程。本课题拟通过LPS刺激巨噬细胞和盲肠结扎穿孔复制脓毒症模型，观察p120基因敲除和过表达后巨噬细胞、脓毒症小鼠肝肺组织TLR4/TRIF-mTOR表达，p120与mTOR、ULK1免疫共定位，自噬相关基因ULK1、Atg5-atg12-atg16和LC3-I/II水平，活性氧ROS、Caspase-1、IL-1β和IL-18等产生，进一步阐明p120-catenin调控巨噬细胞自噬在脓毒症中的分子作用机制。

Sepsis is a common clinical syndrome and treatment problem life-threatening in medical field. p120-catenin is a new member of catenin family, and plays an important role in inflammatory responses, cell proliferation and tumor invasion, and so on. Our previous study found that autophagy protein markers LC3-II were significantly increased following by knocked down p120-catenin in natural state or following by LPS-induced J774A.1 macrophages by making use of siRNA interference technology, and decreased the level of IL-18. Further study shows that p120-catenin can combine with upstream negative regulatory protein mTOR in autophagy signaling pathways. Therefore, we put forward to a hypothesis: p120-catenin could participate in the regulation of macrophages autophagy, and then affecting the process of sepsis. In the present study, making use of LPS induced macrophages and the cecal ligation and puncture established the model of sepsis, we detected the expression of TLR4/TRIF-mTOR, the immunofluorescence co-localization of mTOR and ULK1, the level of autophagy related gene ULK1, Atg5-Atg12-Atg16 and LC3-I/II, ROS, Caspase-1, IL-1β and IL-18 production via using RT-PCR, western blot, Co-IP, immunofluorescence confocal and transmission electron microscope, exploring the molecular mechanism of p120-catenin regulation of macrophage autophagy in sepsis, provide a new field for the immune prevention and treatment of sepsis.