Lin Minling, Huang Ruiting, Li Wanyu, Peng Hui, Chen Jun, Qiu Yongyi, Liu Yi, Chen Lei
School of Traditional Chinese Medicine, Guangdong Pharmaceutical University, Guangzhou, 510006, China.
School of Chinese Medicine, Southern Medical University, Guangzhou, 510515, China.
Arch Biochem Biophys. 2025 Jul;769:110441. doi: 10.1016/j.abb.2025.110441. Epub 2025 May 2.
Studies have shown that dysregulation of intestinal microbial structure and co-metabolic imbalance caused by diet and other factors play important role in MASLD and IBD. However, it is unclear how host-microbial interactions differ in the two diseases, and what potential impact they have on accelerating disease progression. Our study aims to find the disease characteristics in MASLD, IBD and their complication from the perspective of host-microbial metabolism. In our study, mouse models of MASLD, IBD, and MASLD-IBD induced by high-fat diet and dextran sulfate sodium. Detecting the pathological changes of colon and liver. Using 16s rRNA to screen out specific micro-flora, and UPLC-MS to monitor the changes of metabolites in feces. The micro-flora-metabolite co-expression network was constructed by Cytoscape software. The result showed that MASLD-IBD mice aggravate intestinal barrier damage, hepatic steatosis and fibrosis, immune inflammation and other pathological changes. In MASLD-IBD mice, the structural change of gut micro-flora is similar to IBD mice, which significantly reduced the abundance of Actinobacteriota, Desulfobacterota while increasing the abundance of Proteobacteria, and the metabolic disorder include nine metabolic pathways, such as tryptophan, bile acids and short-chain fatty acids, is similar to MASLD mice. Their co-expression network indicates that different specific micro-flora are closely related to the metabolic disorder and disease symptoms of MASLD-IBD mice. Analyzing the relationship between intestinal microbial dysregulation and hoetic co-metabolic imbalance is helpful to understand the mechanism of MASLD and IBD comorbidity, which suggesting that combined liver-gut therapy may be a new method for the treatment of MASLD-IBD complication.
研究表明，饮食等因素引起的肠道微生物结构失调和共代谢失衡在MAFLD和IBD中起重要作用。然而，尚不清楚宿主-微生物相互作用在这两种疾病中有何不同，以及它们对加速疾病进展有何潜在影响。我们的研究旨在从宿主-微生物代谢的角度找出MAFLD、IBD及其并发症的疾病特征。在我们的研究中，用高脂饮食和葡聚糖硫酸钠诱导MAFLD、IBD和MAFLD-IBD的小鼠模型。检测结肠和肝脏的病理变化。使用16s rRNA筛选出特定的微生物群落，并使用超高效液相色谱-质谱联用仪监测粪便中代谢物的变化。用Cytoscape软件构建微生物群落-代谢物共表达网络。结果表明，MAFLD-IBD小鼠的肠道屏障损伤、肝脏脂肪变性和纤维化、免疫炎症等病理变化加重。在MAFLD-IBD小鼠中，肠道微生物群落的结构变化与IBD小鼠相似，放线菌门、脱硫杆菌门的丰度显著降低，而变形菌门的丰度增加，其代谢紊乱包括色氨酸、胆汁酸和短链脂肪酸等九条代谢途径，与MAFLD小鼠相似。它们的共表达网络表明，不同的特定微生物群落与MAFLD-IBD小鼠的代谢紊乱和疾病症状密切相关。分析肠道微生物失调与宿主共代谢失衡之间的关系有助于理解MAFLD和IBD合并症的机制，这表明肝肠联合治疗可能是治疗MAFLD-IBD并发症的一种新方法。
