冠状病毒感染诱发细胞因子风暴导致的重症肺炎是患者死亡的主要原因，然而目前有效平息细胞因子风暴综合征的治疗方法或模式存在空白。动物模型是药物疫苗评价的重要手段，在历次传染病暴发之际，动物模型均发挥至关重要的作用。前期利用易感动物，监测MERS-CoV感染后细胞因子分泌及病理改变，初步建立了MERS-CoV感染诱发的重症肺炎模型，并发现外源性IL-37可显著抑制感染鼠肺组织内炎性因子IL-6、MCP-1等分泌，而IL-37在缓解MERS-CoV感染诱发重症肺炎中的作用机制尚不完全明确。本题拟进一步完善重症肺炎模型，探索IL-37在MERS-CoV感染诱发重症肺炎过程中的作用机制，明确IL-37在感染动物体内发挥生物学活性过程中极化的免疫细胞类型及信号蛋白通路，为冠状病毒感染诱发的重症肺炎的治疗提供新思路。

Coronavirus infection induced cytokines storm, resulting in severe pneumonia is the major cause of death. However, the treatment method or mode to effectively balance the cytokine storm syndrome is blank in clinical practice. Animal model is an important means to evaluate the validity of drug and vaccine. By using susceptible animals, we preliminarily established a model of severe pneumonia induced with MERS-CoV infection in DPP4 murine model, and found that exogenous IL-37 could significantly inhibit the expression of inflammatory cytokines IL-6、MCP-1 in lung tissue. Nevertheless, the mechanism of IL-37 in inflammatory response induced by MERS-CoV infection is not completely clear. In this study, we will establish a perfect model of severe pneumonia induced by MERS-CoV infection, to explore the mechanism of IL-37 in the process of inducing severe pneumonia induced by MERS-CoV infection, clarify the types of immune cells and signal proteins polarized in the process of biological activity in infected animals, and provide new ideas for the treatment of severe pneumonia induced by coronavirus infection.