肠道细菌移位导致的脓毒症是临床常见的致死性并发症，它的发生机理为肠道机械及免疫屏障功能的障碍，其中肠道粘膜免疫损伤扮演着尤为重要的角色。长期以来由于缺乏由粘膜免疫障碍导致细菌移位的理想的动物模型，有关其机制的研究工作一直受到较大的阻碍。我们的前期研究发现严重创伤后肠粘膜固有层树突状细胞（lamina propria dendritic cells, LPDCs）不仅诱导了肠道局部免疫失衡，同时加重了肠道细菌移位，这其中Toll样受体-5（Tlr5）及其下游信号分子起到了关键作用。故课题组拟以对小肠上皮及LPDCs细胞的Tlr5-Myd88信号系统的调控作为切入点，建立一个能将肠道细菌移位作为研究对象、具有可调控性和量化评价功能的小鼠模型。该模型的应用将有利于肠道黏膜免疫研究的深入，更将促进多种肠道细菌移位相关疾病发病新机制的发现及治疗方法的创新。

Sepsis caused by intestinal bacterial translocation is a clinical lethal complication. Its mechanisms include the intestinal mucosal and immune barrier dysfunction, of which mucosal immune injury play a particularly important role. For a long time due to the lack of an ideal animal model of bacterial translocation induced by mucosal immune disorders, such studies have been severely hampered. Our previous study found that Lamina Propria Dendritic Cells (LPDCs) not only induced the intestinal immune imbalance, also aggravated the intestinal bacterial translocation after severe trauma, of which Toll like receptor -5 (Tlr5) and its downstream signaling system plays a key role. Inspired by the regulation of Tlr5-Myd88 signaling system on intestinal epithelial and LPDCs, we plan to establish an mouse model focus on intestinal bacterial translocation, with functions of regulation and quantitative evaluation. Application of this model will be helpful to the study of intestinal mucosal immunity in depth, and promote innovation in discovery of pathogenesis and treatment for a variety of intestinal bacterial translocation related diseases.