肠道细菌移位是急性胰腺炎继发脓毒症(SEPSIS)、多脏器功能衰竭(MOF)的重要因素。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。我们已经发现肠粘膜固有层树突状细胞（lamina propria dendritic cells, LPDCs）功能异常不仅能诱导肠道局部免疫失衡，同时可能加重肠道细菌移位，其中Toll样受体-5（Tlr5）及其下游信号分子起到了关键作用。故课题组拟在急性胰腺炎合并肠道细菌移位的小鼠模型平台上，采用基因敲除（Tlr5-/-和Myd88f/f ）、体外共刺激诱导T细胞分化、LPDCs过继免疫以及生物荧光标记柠檬酸杆菌示踪等技术明确小肠LPDCs细胞的Tlr5-Myd88信号系统调控肠道免疫状态的机制。此项工作不但能够为急性胰腺炎继发免疫失衡提供科学解释，更有可能为今后开发以LPDCs为靶标的新型免疫治疗提供理论依据。

Intestinal bacterial translocation occurs in acute pancreatitis (SAP) patients play an important role in leading to sepsis and MOF, which bend to the mechanism of intestinal machinery and immune barrier function disorder. However the intestinal mucosal immune injury plays a particularly important role. We found that the dysfunction of lamina propria dendritic cells( LPDCs） may induce intestinal immune imbalance and bacterial translocation, and the Toll like receptor 5 (Tlr5) with its downstream signaling molecules may play a key role. We plan to establish a model of SAP combined with intestinal bacterial translocation, then we try to clarify the mechanism of intestinal immune barrier function disorder and bacterial translocation regulated by Tlr5-Myd88 signal system of LPDCs with techniques of knockout(Tlr5-/-和Myd88f/f), co-stimulation to induce T cell differentiation in vitro, adoptive immunity with LPDCs and citrobacter tracing with biological fluorescent. This work will not only provide an explanation for how SAP leading to intestinal bacterial translocation, more likely for the future of providing the theoretical basis for a new type of immunotherapy targets at intestinal LPDCs.