The role of the gut microbiota and microbial metabolites in neuroinflammation,European Journal of Immunology

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The role of the gut microbiota and microbial metabolites in neuroinflammation
European Journal of Immunology ( IF 4.5 ) Pub Date : 2020-11-14 , DOI: 10.1002/eji.201847807
Stefanie Haase ₁ , Nicola Wilck _{2,

3,

4,

5,

6} , Aiden Haghikia ₇ , Ralf Gold ₈ , Dominik N. Mueller _{3,

4,

5,

6} , Ralf A. Linker ₁

Affiliation

Recent literature indicates a potential importance of the gut microbiota for immune‐mediated diseases. For instance, decreased diversity of commensals or an outgrowth of some bacterial strains, referred to as gut dysbiosis, was recently linked to hypertension, colitis, lupus, rheumatoid arthritis, and multiple sclerosis (MS). Studies in experimental autoimmune encephalomyelitis (EAE) as pivotal animal model of MS revealed a potential importance of microbial metabolites, including short‐chain fatty acids or tryptophan metabolites. Both metabolites may influence the disease by modulation of the immune system, mainly by inducing Treg. These studies prompted researchers to investigate the contribution of the gut microbiota and microbial metabolites in the pathogenesis of MS. This review summarizes recent findings on the gut microbiota in MS patients and discusses the potential mechanisms how microbial metabolites may affect neuroinflammation. Many of these studies have been performed in the EAE model and were later reversely translated to humans. We also give a short summary on dietary high‐salt effects on microbiota components and discuss the potential relevance of high‐salt as a risk factor in MS.

中文翻译：

肠道菌群和微生物代谢产物在神经炎症中的作用

最近的文献表明肠道菌群对于免疫介导的疾病具有潜在的重要性。例如，最近由于食欲不振或某些细菌菌株的生长（称为肠道营养不良），导致高血压，结肠炎，狼疮，类风湿关节炎和多发性硬化症（MS）。作为MS关键动物模型的实验性自身免疫性脑脊髓炎（EAE）的研究表明，微生物代谢产物（包括短链脂肪酸或色氨酸代谢产物）具有潜在的重要性。两种代谢物都可能通过调节免疫系统（主要是通过诱导Treg）来影响疾病。这些研究促使研究人员研究肠道微生物群和微生物代谢产物在MS发病机理中的作用。这篇综述总结了MS患者肠道菌群的最新发现，并讨论了微生物代谢产物如何影响神经炎症的潜在机制。这些研究中有许多是在EAE模型中进行的，后来被反向翻译成人类。我们还简要介绍了饮食中高盐对微生物群成分的影响，并讨论了高盐作为MS危险因素的潜在相关性。

更新日期：2020-12-12

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