肠系膜脂肪组织结构及功能的异常与肠道慢性炎症相互作用，参与了克罗恩病(CD)的疾病进程。本课题组既往研究表明，CD肠系膜脂肪细胞存在结构及功能异常，肠系膜脂肪增生与CD疾病严重程度及术后复发显著相关。改善肠系膜脂肪细胞的功能明显减轻CD模型小鼠的肠道炎症。本课题在前期研究的基础之上，运用分子生物学及分子免疫学等技术，从肠系膜脂肪细胞脂代谢障碍及模式识别受体异常的角度探讨CD肠系膜脂肪细胞功能障碍的机制，并以缺氧诱导因子(HIF)通路为切入点，探寻肠系膜脂肪组织炎症发生的根源以及可能的调控机制，以期揭示肠系膜脂肪细胞功能障碍在CD肠道炎症发生及发展中的作用及机制，为阐释 CD 病理生理提供理论依据，为CD的防治提供新的靶点。

Mesenteric adipose tissue is a unique feature of Crohn's disease (CD), the role played by mesenteric adipose tissue in the pathogenesis of CD has recently been recognized. It is currently accepted that mesenteric adipose fat is important in disease development and progression of CD. The crosstalk between mesentetic adipose tissue and bowel is mainly through the secretion of adipokines and cytokines from mesenteric adipocyte although the detailed information remains unknown. Work of our group have indicated that the hypertrophic mesenteric adipose tissue which is found in patients with CD, is associated with disease process, disease activity, and disease recurrence of CD. In addition, we found that improvement of the mesenteric function of adipocyte is related to attenuated animal colitis. We proposed this project based on our previous work, we aimed to explore the underlying mechanisms metabolic disorders and pattern recognition receptors abnormal of mesenteric adipocyte, and we hypothesized that HIF pathway may be implicated in the disorders of mesenteric adipocyte. The histopathology, molecular biology and molecular immunology would be used in this study. Our study would provide data to understand the pathogenesis of CD and suggest a novel target for the management of CD.