Protection of Fecal Microbiota Transplantation in a Mouse Model of Multiple Sclerosis.

Kanglan Li,Xiaoping Peng,Shouchao Wei,Yingren Mai,Zhou Liu,Guoda Ma,Li Hu,Xiaojian Yin,Haihong Zhou,Zhongkai Huang,Xingxing Cao,Chunmei Jiang,Huiliang Li,Bin Zhao

doi:10.1155/2020/2058272

Abstract

Given the growing evidence of a link between gut microbiota (GM) dysbiosis and multiple sclerosis (MS), fecal microbiota transplantation (FMT), aimed at rebuilding GM, has been proposed as a new therapeutic approach to MS treatment. To evaluate the viability of FMT for MS treatment and its impact on MS pathology, we tested FMT in mice with experimental autoimmune encephalomyelitis (EAE), a mouse model of MS. We provide evidence that FMT can rectify altered GM to some extent with a therapeutic effect on EAE. We also found that FMT led to reduced activation of microglia and astrocytes and conferred protection on the blood-brain barrier (BBB), myelin, and axons in EAE. Taken together, our data suggest that FMT, as a GM-based therapy, has the potential to be an effective treatment for MS.

Highlights

Multiple sclerosis (MS) commonly occurs as a progressive central nervous system (CNS) disease, characterized by inflammation, demyelination, and axonal loss in the brain and spinal cord [1]
The Shannon index was significantly increased for gut microbiota (GM) in EAE mice compared to normal controls (4:38 ± 0:15 vs. 3:89 ± 0:26, p = 0:008113), indicating altered GM diversity in EAE; an in-between value was discovered in fecal microbiota transplantation (FMT)-treated EAE mice without statistical significance (Figure 1(a)), suggesting that FMT attenuated the increase in the Shannon index caused by the development of EAE
To assess the influence of FMT on myelin and axons, we examined the expression of myelin basic protein (MBP), which is expressed in myelin, and neurofilament light chain protein (NF-L), whose release reflects axonal damage, in brain tissue

Summary

Introduction

Multiple sclerosis (MS) commonly occurs as a progressive central nervous system (CNS) disease, characterized by inflammation, demyelination, and axonal loss in the brain and spinal cord [1]. T cell-mediated inflammatory pathology and genetic factors are closely involved in the development of MS, causing damage to myelin sheaths surrounding neuronal axons and accumulation of neurological deficits [2,3,4]. Study has shown that transplanting the intestinal microbiota of autism spectrum disorder patients into germ-free mice and that colonization of the microbiota induced typical autism spectrum disorder behaviors [6]. Germ-free mice developed severe MS symptoms after microbiota transplants from MS patients compared with transplanted healthy controls [7]. Accumulating new evidence points to a link between altered intestinal microbiota and MS pathogenesis [10,11,12,13,14,15]

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Discussion

Conclusion