肠道菌群在神经系统疾病发病中的作用已有大量报道，但是联系脑-肠轴的具体机制尚未完全阐明，缺乏有力证据。因此，我们以神经炎症性疾病为研究对象，利用该类疾病的经典模型-实验性自身免疫性脑脊髓炎（EAE）小鼠模型，采用多种组学技术，探讨肠道菌群紊乱对该疾病的作用，并深入研究肠道菌群紊乱是如何通过中间介质-肠道代谢产物影响该疾病中致病细胞-Th17细胞的分化及功能，从而参与疾病发病的。并且，我们还将收集多发性硬化症病人的标本，对肠道菌群以及代谢产物在病人发病中的作用进行深入探索，在揭示肠道菌群及代谢产物作用机制的同时检测并验证其是否可以作为多发性硬化症病人的诊断标志物。综上，该项目研究成果将揭示脑肠轴中肠道菌群对中枢神经系统作用的免疫学机制，为深入理解脑肠轴中的互作关系提供理论基础；同时结合临床标本的研究为该疾病的临床诊断以及干预新方案的提出提供思路和依据。

The role of intestinal microbiota in the pathogenesis of has yet been elucidated, but the underlying mechanism is not clear. By using a classical model of neuronal Inflammation- experimental autoimmune encephalomyelitis (EAE), we plan to study how dysibiosis-the imbalance of intestinal mcrobiota cause neuronal inflammation by affecting the differentiation and function of the pathogenic Th17 cells through microbial metabolites. In addition, we will use clinical samples from multiple sclerosis patients to further explore whether there is a correlation between these metabolites and the pathogenesis of the diseases. The mechanisms of how microbial metabolites contribute to neuronal inflammation elucidated in this project will eventually results in new diagnostic markers and new intervention methods for neuronal inflammation.