脂肪巨噬细胞（ATMs）在重症急性胰腺炎（SAP）发病中占有重要地位。我们前期研究发现在肥胖鼠SAP急性期ATMs数量意外的持续减少，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：1）以细胞凋亡为基础，进一步探索诱导SAP后ATMs数量减少的调控机制。2）寻找准确描述ATMs功能状态以评估SAP状态的方法：以脂质代谢、炎症反应及凋亡的调控交叉点—溶酶体为靶点，观察诱导SAP前后ATMs溶酶体的功能状态变化及其与炎症发展的关系，以了解ATMs在肥胖相关SAP中的作用。3）研究溶酶体cathpsin B-NLRP3炎症体途径调控肥胖相关SAP炎症加重与ATMs减少的可能机制：溶酶体的关键水解酶cathpsin B可激活NLRP3炎性体,后者进一步促进细胞凋亡及炎症因子释放。深入研究该途径，对解释肥胖相关SAP炎症加重与ATMs减少这一矛盾现象具有重要意义。

Adipose tissue macrophages (ATMs) play key roles in the development of severe acute pancreatitis (SAP). Our previous data showed that the number of ATMs was declined significantly in acute response stage of obesity related SAP. In this study, we aim to resolve the mechanisms of conflicts between the “decreased” number of ATMs and “increased” inflammation. Firstly, we explore the molecular mechanisms of depletion in the number of ATMs during SAP based on apoptosis. Secondly, we investigate the markers for evaluating ATMs' functional status during SAP. In obesity, lysosome is associated with the modulation of lipid metabolism, inflammation, and apoptosis. We presume that the functional states of lysosome and the relationship between lysosome and inflammation may be prospective in description of the role of ATMs in the pathogenesis of obesity related SAP. Finally, we investigate the underlying mechanism that lysosome/ cathepsin B-The NLR family, pyrin domain-containing 3 (NLRP3) inflammasome pathway regulate both the inflammation development of SAP and the “decreased” number of ATMs. NLRP3 inflammasome not only induces the apoptosis process, but also promotes production of inflammatory factors. Therefore, our study about lysosome/ cathepsin B-NLRP3 inflammasome pathway would provide further understanding for the mechanisms of the above conflict.