Evidence map›Paper›PMID 31784260›Full record

ArticleCell host & microbe2019

Oral Administration of miR-30d from Feces of MS Patients Suppresses MS-like Symptoms in Mice by Expanding Akkermansia muciniphila.

Shirong Liu, Rafael M Rezende, Thais G Moreira, Stephanie K Tankou, Laura M Cox, Meng Wu, Anya Song, Fyonn H Dhang, Zhiyun Wei, Gianluca Costamagna and 1 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell host & microbe, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 134 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
134citing papers in PubMed, 5 pooled it
8.2field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

134 citing papers in PubMed, 5 syntheses or guidelines pooled it, 201 citations in OpenAlex.

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74 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 1 country.

Shirong LiuAnn Romney Center for Neurologic Diseases, Department of Neurology, Partners Multiple Sclerosis Center, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA; Evergrande Center for Immunologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA 02115, USA. Electronic address: sliu22@bwh.harvard.edu.
Rafael M RezendeAnn Romney Center for Neurologic Diseases, Department of Neurology, Partners Multiple Sclerosis Center, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA; Evergrande Center for Immunologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA 02115, USA.
Thais G MoreiraAnn Romney Center for Neurologic Diseases, Department of Neurology, Partners Multiple Sclerosis Center, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA; Evergrande Center for Immunologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA 02115, USA.
Stephanie K TankouAnn Romney Center for Neurologic Diseases, Department of Neurology, Partners Multiple Sclerosis Center, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA; Evergrande Center for Immunologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA 02115, USA.
Laura M CoxAnn Romney Center for Neurologic Diseases, Department of Neurology, Partners Multiple Sclerosis Center, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA; Evergrande Center for Immunologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA 02115, USA.
Meng WuDepartment of Microbiology and Immunobiology, Harvard Medical School, Boston, MA 02115, USA.
Anya SongAnn Romney Center for Neurologic Diseases, Department of Neurology, Partners Multiple Sclerosis Center, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA; Evergrande Center for Immunologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA 02115, USA.
Fyonn H DhangAnn Romney Center for Neurologic Diseases, Department of Neurology, Partners Multiple Sclerosis Center, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA; Evergrande Center for Immunologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA 02115, USA.
Zhiyun WeiAnn Romney Center for Neurologic Diseases, Department of Neurology, Partners Multiple Sclerosis Center, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.
Gianluca CostamagnaAnn Romney Center for Neurologic Diseases, Department of Neurology, Partners Multiple Sclerosis Center, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA; Evergrande Center for Immunologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA 02115, USA.
Howard L WeinerAnn Romney Center for Neurologic Diseases, Department of Neurology, Partners Multiple Sclerosis Center, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA; Evergrande Center for Immunologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, MA 02115, USA.
Brigham and Women's Hospital · USHarvard University · US

Funding

Gut Microbiota in Patients with Multiple SclerosisR01NS087226 · NINDS · BRIGHAM AND WOMEN'S HOSPITAL · PI WEINER, HOWARD L · 2014 to 2018
$1.9M
NINDS NIH HHS R01 NS087226
6 · The paper itself

Abstract

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.

Indexed as

Encephalomyelitis, Autoimmune, ExperimentalFecal Microbiota TransplantationVerrucomicrobiaAdministration, OralAkkermansiaAnimalsFecesGastrointestinal MicrobiomeHost Microbial InteractionsHumansLactaseMiceMice, Inbred C57BLMicroRNAsMultiple SclerosisT-Lymphocytes, RegulatoryLactaseMicroRNAsMirn30d microRNA, mouseAkkermansia muciniphilaautoimmune diseasesexperimental autoimmune encephalomyelitisfecal transplantationhost-microbe interactionmicrobiomemicroRNAmicrovesiclemultiple sclerosisregulatory T cell

Identifiers

PMID31784260
PMCPMC6948921
OpenAlexW2989647074

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.