Gut Microbiota from Multiple Sclerosis patients triggers spontaneous autoimmune encephalomyelitis in mice --16S data--

The commensal microbiota has emerged as a key factor influencing human
health and has been associated with several diseases, including those of
the central nervous system (CNS). To investigate the role of the
microbiome in multiple sclerosis (MS), a complex autoimmune disorder
shaped by a multitude of genetic and environmental factors, we recruited a
cohort of 34 monozygotic twin pairs discordant for MS, and compared their
gut microbial composition by 16S ribosomal RNA sequencing of stool
samples. While no major differences in the microbial profiles between
MS-affected twins and their healthy co-twins were detected, a significant
increase in some taxa (including Akkermansia) was seen in affected
untreated subjects. To search for possible functional differences, we used
a transgenic mouse model, in which spontaneous anti-CNS autoimmunity is
dependent on the commensal gut flora. Germ-free mice colonized with
microbiota from MS-affected twins, developed the MS-like disease with a
significantly higher incidence than mice colonized with healthy
twin-derived microbiota. Although alpha diversity was reduced compared to
human donors, the microbial profiles of the colonized mice showed high
intraindividual, remarkable temporal stability and a high transfer rate,.
Analysis of the transplanted mouse microbiome at the level of individual
taxa revealed several differences, including a significantly reduced
abundance of the potentially autoimmune-protective genus Sutterella in
mice colonized with MS-twin-derived microbiota. These findings provide
first evidence that MS-derived microbiota contain factors that precipitate
an MS-like autoimmune disease in a transgenic mouse model. This model
lends itself to identify protective and pathogenic microbial component in
human MS.