Gut inflammation and dysbiosis in human motor neuron disease

Amyotrophic lateral sclerosis (ALS) is a systemic disorder that involves dysfunction of multiple organs. Growing evidence has shown that neurodegenerative disorders with gut dysbiosis affect the central nervous system via pro‐inflammatory mediators thus impacting gut‐brain communications. We have de...

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Bibliographic Details
Published inPhysiological reports Vol. 5; no. 18; pp. e13443 - n/a
Main Authors Rowin, Julie, Xia, Yinglin, Jung, Barbara, Sun, Jun
Format Journal Article
LanguageEnglish
Published United States John Wiley & Sons, Inc 01.09.2017
John Wiley and Sons Inc
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Summary:Amyotrophic lateral sclerosis (ALS) is a systemic disorder that involves dysfunction of multiple organs. Growing evidence has shown that neurodegenerative disorders with gut dysbiosis affect the central nervous system via pro‐inflammatory mediators thus impacting gut‐brain communications. We have demonstrated dysbiosis and increased intestinal permeability in the SOD1G93A ALS mouse model. In this study, we comprehensively examined the human gut microbiome in stool samples and evaluated infection and markers of intestinal inflammation in five patients with ALS and motor neuron disorders. Five patients we studied all had alteration in their gut microbiome characterized by a low diversity of the microbiome, compared to healthy cohorts with relatively intact abundance. Firmicutes and Bacteroidetes are the two major members of bacteria at the phylum level. Low Ruminococcus spp. occurred in three patients with low Firmicutes/Bacteroidetes (F/B) ratio. A majority of patients had signs of intestinal inflammation. This is the first comprehensive examination of inflammatory markers in the stool of ALS patients. Studies in gut health and microbiome related to the onset and progression of ALS may reveal novel therapeutic targets for disease modulation. We report intestinal inflammation and dysbiosis in human amyotrophic lateral sclerosis (ALS). Our study may help explain dysbiosis (imbalanced microbiomes) that negatively impacts individuals in human diseases.
Bibliography:Funding Information
We acknowledge the NIDDK/National Institutes of Health grant R01 DK105118 to Jun Sun.
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Part of the material is contained within an abstract that has been selected to present at the AANEM 64th Annual Meeting in Phoenix, Arizona, September 14, 2017.
ISSN:2051-817X
2051-817X
DOI:10.14814/phy2.13443