炎症性肠病中的巨噬细胞糖代谢重编程

Macrophage Glucose Metabolism Reprogramming in Inflammatory Bowel Disease

摘要: 炎症性肠病(IBD)是肠道免疫系统过度激活所致的一种慢性炎症性疾病。巨噬细胞在肠道免疫中发挥重要作用，其极化表型及功能受细胞代谢的调控。在炎症性肠病的发生发展中，巨噬细胞表现出明显的糖代谢重编程，即出现从氧化磷酸化向糖酵解转变，并且出现磷酸戊糖途径的上调、三羧酸循环受损，促进M1型巨噬细胞的极化及炎症因子的表达，进而加重炎症性肠病。这一代谢重编程受多种信号分子的调节，肠道菌群及代谢物，包括短链脂肪酸、色氨酸、胆汁酸等也在这一代谢过程中发挥不可替代的作用。因此，对炎症性肠病中的巨噬细胞糖代谢重编程进行阐述，不仅深化了炎症性肠病免疫代谢理论的理解，也为开发干预代谢通路缓解炎症性肠病的新治疗策略提供重要科学依据。

Abstract: Inflammatory bowel disease (IBD) is a chronic inflammatory disease caused by abnormal activation of the intestinal immune system. Macrophages play an important role in intestinal immunity, and their polarized phenotype and function are regulated by cellular metabolism. In the development and progression of inflammatory bowel disease, macrophages exhibit a significant reprogramming of glucose metabolism, shifting from oxidative phosphorylation to glycolysis, with upregulation of the pentose phosphate pathway and impaired tricarboxylic acid cycle. This further promotes M1 macrophage polarization and the expression of inflammatory cytokines, exacerbating inflammatory bowel disease. This metabolic reprogramming is regulated by multiple signaling molecules, and gut microbiota and metabolites such as short-chain fatty acids, tryptophan, and bile acids also play irreplaceable roles in this metabolic process. Therefore, elucidating the reprogramming of macrophage glucose metabolism in inflammatory bowel disease not only deepens our understanding of the immuno-metabolic theory underlying inflammatory bowel disease but also provides crucial scientific evidence for developing novel therapeutic strategies that target metabolic pathways to alleviate inflammatory bowel disease.