通常认为蠕虫感染或蠕虫来源的分子可通过诱导机体产生2型免疫应答来负向调控肥胖诱导的1型炎性反应。然而，有新观点提出慢性血吸虫感染会诱导过度2型炎症应答（尤指IL-13高表达），反而加重宿主的肝脂代谢异常。我们的前期工作提示，日本血吸虫感染B6小鼠可下调肝miR-802的表达，致靶基因Prkab1表达上升，激活AMPK通路，以抑制肝脂质合成。进一步发现，低浓度的IL-13刺激肝细胞可通过IL-13Rα1受体激活下游STAT6信号从而下调miR-802的表达，而高浓度的IL-13作用可引起IL-13Rα2转录增强，反而使得miR-802表达升高。本研究拟在血吸虫感染小鼠模型上研究不同强度的IL-13利用不同的IL-13受体，通过STAT6依赖或非依赖途径来调控miR-802的表达，以抑制或增加肝脂质合成。深入阐明2型炎症应答机制将对临床诊治脂肪肝等疾病给予一定的指导作用。

It is well known that helminth infections or helminthes-derived molecules can induce host type-2 immune response, which can protect against obese characteristic of the dominant type-1 inflammation. Up to now, there is a novel view that chronic schistosome infection can produce the excessive type 2 inflammation (especially the amount of IL-13) to exacerbate NAFLD. Our previous studies found that Schistosoma japonicum infection results in downregulating hepatic miR-802, which can target Prkab1 and activate AMPK pathway. AMPK activation contributes to inhibiting hepatic lipogenesis. In addition, we also found that low concentration of IL-13 downregulates the expression of miR-802, whereas high concentration of IL-13 can induce miR-802 expression. Thus, in this project, we would like to observe the exact roles of IL-13 in the interaction of host infection and metabolism, that is, the different intense of IL-13 including concentration and duration time through the corresponding IL-13 receptors might regulate the different expression of miR-802 to mediate the distinct outcome of hepatic lipid metabolism. This study will help us to understand the mechanisms of type-2 inflammation reaction in host metabolism.