补体因子D通过调控肠道细菌及其代谢产物影响炎症性肠病相关巨噬细胞分化和功能的作用机制研究

炎症性肠病（inflammatory bowel disease,IBD）是一种慢性复发性炎症性肠道疾病。目前其发病原因和机制尚未完全明确，但是许多报告指出IBD的发生发展与肠道菌群/细菌代谢物和肠免疫细胞的耐受状态存在密切关系。尽管如此，人们并不清楚哪些肠道细菌/细菌代谢物与肠炎发生发展有关，以及这些肠道细菌/细菌代谢物如何影响肠炎发生发展的。因此搞清肠炎相关免疫细胞分化及调控机理，能够推动IBD的预防和治疗。补体因子D(complement factor D, CFD)在肠上皮细胞高表达，具有杀灭细菌作用。关键的是利用CFD肠条件敲除鼠，发现在DSS诱导的肠炎模型中CFD能抑制肠炎的发生，同时CFD抑制炎症性巨噬细胞在肠组织聚集。因此，搞清CFD调控肠炎相关巨噬细胞分化和功能的机制，不仅对解开肠微生态在IBD发生发展中的作用机理提供依据，也为发展新的肠炎预防和治疗策略奠定坚实的基础。

Inflammatory bowel disease (IBD), including ulcerative colitis and Crohn’s disease, is a chronic and relapsing inflammatory disorder of the intestine. Although its incidence is increasing globally, the precise etiology and regulation mechanism remain unclear. Recent advances found that IBD is related with gut bacteria/bacterial metabolites and the tolerance status of gut immune cells. However, it is still unclear which and how of gut bacteria/bacterial metabolites regulated the occurrence and development of IBD. Complement factor D(CFD）belongs to complement system and has a high-level expression in gut epithelial cells. Importantly, CFD was reported to have the ability of bacteria-killing. Furthermore, CFDKO mice were more sensitive to DSS-induced colitis, and CFD inhibited the aggregate of inflammatory macrophages in colon lamina propria tissue. So, it is critical to understanding the mechanism of the differentiation and functions of macrophages regulated by CFD, which will not only provide a basis for unraveling the mechanism of action of intestinal microecology in the occurrence and development of IBD, but also lay a solid foundation for the development of new prevention and treatment strategies for IBD.