巨噬细胞在重症急性胰腺炎（SAP）发病中占重要地位。肥胖是SAP的高危因素。由于肥胖时脂肪组织巨噬细胞（ATMs）可以占到脂肪组织细胞总数的40%以上，有理由相信ATMs在肥胖相关的SAP发病中占有重要地位。然而我们前期工作发现诱导SAP后ATMs的数量出现意外的持续减少，这与局部/全身炎症进展状态相矛盾。为探究这一矛盾产生的原因，本课题拟检测SAP诱导前后ATMs的增殖、凋亡、前脂肪细胞转化及异位迁徙水平以寻找ATMs数量减少的原因；探讨比M1/M2极化改变更为重要的ATMs参与炎症的功能性调控，判断ATMs在肥胖诱导SAP发病中的作用地位。

Macrophages play key roles in the development of severe acute pancreatitis（SAP）. Obesity is a significant risk factor to SAP. Adipose tissue macrophages（ATMs）constitutes 40% of cells in adipose tissue.Therefore, ATMs are presumably much participated in SAP. However, our previous data showed the number of ATMs was declined significantly after the onset of SAP. In this study, we aim to resolve the mechanism of conflicts between the "decreased" numbers of ATMs and "aggravated" inflammation. Firstly, we explore the cause of the depletion in numbers of ATMs during SAP. Our experiment include the investigation of apoptosis，proliferation，transformation and migration of ATMs. Moreover，we have observed that ATMs presented as M1 polarization in adipose tissue during obesity whether or not induced by SAP. Therefore，M1/M2 polarization is insufficient to represent the characteristics of ATMs in obesity-related SAP. The major function of ATMs includes modulation of lipid metabolism and immune regulation, which have recently been reported to be both associated with the lysosome. Therefore, we presume that the functional states of lysosome may be prospective in description of the role of ATMs in the pathogenesis of SAP. A better understanding of the role of ATMs in obesity-related SAP would provide important insights into pathogenesis and may generate new therapeutic approaches.