单核巨噬细胞极化是脓毒症免疫功能障碍的重要部分，但其分子机制尚不明确。Siglec-E多表达于单核巨噬细胞表面，我们前期研究显示，脓毒症小鼠巨噬细胞表面Siglec-E升高，且体内干扰Siglec-E后，脓毒症小鼠死亡率明显升高。我们推测Siglec-E参与脓毒症巨噬细胞的极化过程。课题采用RAW264.7细胞及Siglec-E基因敲除小鼠，以LPS及盲肠结扎穿孔术制备脓毒症模型，通过Siglec-E RNA干扰及过表达检测巨噬细胞极化指标来验证Siglec-E对巨噬细胞极化的作用；进一步采用JAK1-STAT6抑制剂来证实Siglec-E发挥作用受到JAK1-STAT6通路的调控。本课题旨在证实Siglec-E通过JAK1-STAT6通路调节脓毒症巨噬细胞M2极化，也证实JAK1-STAT6是Siglec-E发挥免疫调节的重要分子通路，为脓毒症治疗提供新方向。

Macrophage polarization, as a major participant of immune dysfunction in sepsis, has an ambiguous pathogenesis until now. Siglec-E is a molecular mostly expressed on the surface of macrophage, and our previous study showed that Siglec-E on macrophages in sepsis was up-regulated, and the survival of septic mice decreased when the expression of Siglec-E was inhibited. From those phenomena, we suppose that Siglec-E is involved in the polarization of macrophage in sepsis. RAW264.7 cells and Siglec-E knock out mice were employed, and the models of sepsis were prepared by LPS and cecal ligation and puncture (CLP). Siglec-E RNA was interfered or over-expressed, then macrophage polarization was tested to confirm the role of Siglec-E. After that, JAK1-STAT6 inhibitors were used to verify the involvement of JAK1-STAT6 signal pathway. The purpose of this project is to elucidate that Siglec-E regulates the macrophage polarization in sepsis through JAK1-STAT6 signal pathway, which provides a new direction in the treatment of sepsis.