炎症因子是重症急性胰腺炎（severe acute pancreatitis, SAP）发生和进展的重要因素，也是早期诊断SAP和预测其严重性的指标。 趋化因子Fractalkine（FKN）既有趋化分子的活性又能发挥粘附分子的作用，这种独特的双重功效使其参与了多种炎症反应，造成组织损伤。目前国内外还没有关于FKN及其受体CX3CR1参与SAP发生发展的报道。我们前期研究发现，FKN在大鼠SAP模型的血清和胰腺组织中均过度表达，参与了SAP炎症反应。本课题拟在前期基础上：1）明确FKN在SAP发生和发展中的具体表达形式；2）FKN／CX3CR1的过表达及其沉默后对Jak/Stat信号传导通路的调节效应；3）沉默FKN／CX3CR1功能后，对胰腺及胰腺外损伤器官肺脏和肾脏的影响。通过上述研究，阐明FKN在SAP中的作用及机制，为FKN能否作为判断SAP发生和预测其严重性的指标，提供实验依据。

At the early state of sever acute pancreatitis (SAP), some of the inflammatory cells and pancreatic tissues release inflammatory cytokines. The inflammatory cytokines play an important role in the progression of SAP. At the same time, inflammatory cytokines are available markers for early diagnosis and prediction of the severity of SAP. Because of Fractalkine (FKN) unique biological structure, it has the dual role of chemoattractant and adhesion, which also makes the role of FKN in inflammation concerned more and more. Accumulating evidence indicates that FKN is involved in the pathogenesis of various inflammatory disorders and leads to tissue injury. At present, there is no reported that FKN is involved in the occurrence and development of SAP. In our preliminary study, FKN was overexpression in serum and tissues of SAP rat models. In this study, we aim to solve the following questions ：firstly, we will identify which form of FKN is to participate and how to effect the occurrence and development of SAP. Secondly, how can FKN and its receptor CX3CR1 effect on Janus kinase/signal transducers and activators of transcription (Jak/Stat) signaling pathways when overexpressed or silenced. At last, we will observe the changes of the pancreas and other injury organs (such as lung and kidney) in SAP rat models after silencing the FKN functions. Through this research, we will try to clarify the effect and mechanism of FKN in SAP and make it clear whether FKN can act as an early marker to predict SAP and the severity of SAP.