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Oral administration of miR-30d from feces of MS patients suppresses MS-like symptoms in mice by expanding Akkermansia muciniphila
- Source :
- Cell Host Microbe
- Publication Year :
- 2019
-
Abstract
- Summary Fecal transfer from healthy donors is being explored as a microbiome modality. MicroRNAs (miRNAs) have been found to affect the microbiome. Multiple sclerosis (MS) patients have been shown to have an altered gut microbiome. Here, we unexpectedly found that transfer of feces harvested at peak disease from the experimental autoimmune encephalomyelitis (EAE) model of MS ameliorates disease in recipients in a miRNA-dependent manner. Specifically, we show that miR-30d is enriched in the feces of peak EAE and untreated MS patients. Synthetic miR-30d given orally ameliorates EAE through expansion of regulatory T cells (Tregs). Mechanistically, miR-30d regulates the expression of a lactase in Akkermansia muciniphila, which increases Akkermansia abundance in the gut. The expanded Akkermansia in turn increases Tregs to suppress EAE symptoms. Our findings report the mechanistic underpinnings of a miRNA-microbiome axis and suggest that the feces of diseased subjects might be enriched with miRNAs with therapeutic properties.
- Subjects :
- Encephalomyelitis, Autoimmune, Experimental
Multiple Sclerosis
Regulatory T cell
Administration, Oral
Microbiology
T-Lymphocytes, Regulatory
Article
03 medical and health sciences
Feces
Mice
0302 clinical medicine
Verrucomicrobia
Virology
medicine
Animals
Humans
Microbiome
030304 developmental biology
Lactase
0303 health sciences
biology
Host Microbial Interactions
Microvesicle
Multiple sclerosis
Experimental autoimmune encephalomyelitis
Akkermansia
Fecal Microbiota Transplantation
biology.organism_classification
medicine.disease
Gastrointestinal Microbiome
Mice, Inbred C57BL
MicroRNAs
medicine.anatomical_structure
Immunology
Parasitology
030217 neurology & neurosurgery
Akkermansia muciniphila
Subjects
Details
- Language :
- English
- Database :
- OpenAIRE
- Journal :
- Cell Host Microbe
- Accession number :
- edsair.doi.dedup.....df2b7562429c100084cfb1b6fe833603