肠道区域树突状细胞（dendritic cells, DCs）亚群在维持肠道免疫稳态、炎症发生等生理与病理过程中起着重要作用。DC细胞的功能、表型与定居的肠道微环境，尤其是肠道微生物代谢微环境密切相关。近年来，肥胖及其引起的慢性炎症疾病已成为我国乃至全球的重要社会问题，但肥胖如何通过影响肠道免疫微环境，尤其影响肠道DC细胞亚群稳态，从而引起炎症的机制仍不清楚。本课题拟利用高脂饮食（high fat diet, HFD）肥胖模型，通过气-质联用分析及相关免疫技术，分析肥胖对肠道内微生物代谢产物短链脂肪酸和DC细胞亚群的影响，探寻短链脂肪酸与肠道DC细胞亚群稳态间的关系，并结合免疫性肠炎模型，深入研究短链脂肪酸调控肠道DC细胞的作用及机制，以阐明肠道代谢微环境对肠道区域DC细胞独特的调节机制，及与肥胖相关炎症肠病的关系，为更好地了解肠道区域免疫特性及治疗相关疾病奠定理论基础。

Mucosal dendritic cells (DCs) play vital roles in maintaining immune homeostasis and promoting inflammation in the gut. The biological functions and phenotypes of these DCs are largely depended on the resident microenvironment, especially tightly associated with intestinal flora and its metabolism. In recent decades, the population with obesity and its induced chronic inflammatory diseases dramatically increased and cost billions of dollars in China and other western countries. But, up to now, the roles of intestinal flora and mucosal dendritic cell subsets in obesity promoted inflammation are still not well explored. Here, we use high fat diet (HFD) feeding mice as obesity model to explore the effects of obesity on intestinal flora, its metabolites short chain fatty acids (SCFAs) and DC subsets by using highthroughput sequencing, gas chromatography-mass spectrometry and immunological methods. Moreover, we will study the contribution of SCFAs in regulating mucosal DCs by using HFD mice and dextran sulfate sodium induced colitis models. If this study were well done, it will demonstrated the potential mechanisms of gut microenvironment in regulating mucosal DCs, and its contribution in obesity induced inflammatory diseases. It will also be helpful in designing the strategies to treat these diseases.