Evidence map›Paper›PMID 31061496›Full record

ArticleScientific reports2019

The role of gut microbiota in shaping the relapse-remitting and chronic-progressive forms of multiple sclerosis in mouse models.

K Alexa Orr Gandy, Jiajia Zhang, Prakash Nagarkatti, Mitzi Nagarkatti

Abstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

62 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Changes in Gut Microbiota and Multiple Sclerosis: A Systematic Review.International journal of environmental research and public health · 2023
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2 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

4 authors.

K Alexa Orr GandyDepartment of Pathology, Microbiology and Immunology, University of South Carolina, School of Medicine, Columbia, USA.ORCID http://orcid.org/0000-0003-2481-6269
Jiajia ZhangEpidemiology and Biostatistics, Arnold School of Public Health, University of South Carolina, Columbia, USA.
Prakash NagarkattiDepartment of Pathology, Microbiology and Immunology, University of South Carolina, School of Medicine, Columbia, USA.
Mitzi NagarkattiDepartment of Pathology, Microbiology and Immunology, University of South Carolina, School of Medicine, Columbia, USA. Mitzi.Nagarkatti@uscmed.sc.edu.

Funding

Targeting early ceramide elevation in pre-symptomatic eczemaP20GM103641 · NIGMS · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI ENOS, REILLY, NAGARKATTI, PRAKASH S · 2012 to 2023
$20.7M
Use of Resveratrol to treat experimental multiple sclerosisP01AT003961 · NCCIH · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI HOFSETH, LORNE J · 2007 to 2018
$14.2M
Epigenetic Mechanisms of T Cell Dysregulation in PTSDR01AI129788 · NIAID · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI NAGARKATTI, MITZI · 2017 to 2021
$2.4M
Role of natural indoles in experimental autoimmune encephalomyelitisR01AT006888 · NCCIH · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI NAGARKATTI, MITZI · 2011 to 2015
$2.0M
AhR ligands in epigenetic dysregulation of T cellsR01AI123947 · NIAID · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI NAGARKATTI, MITZI, NAGARKATTI, PRAKASH S · 2017 to 2021
$1.8M
Immunopathological basis of PTSDR01MH094755 · NIMH · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI NAGARKATTI, PRAKASH S · 2011 to 2015
$1.7M
MicroRNA regulation of EAE by resveratrolF32AT008539 · NCCIH · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI GANDY, K ALEXA · 2014 to 2016
$177k
NCCIH NIH HHS F32 AT008539NCCIH NIH HHS P01 AT003961NCCIH NIH HHS R01 AT006888NIAID NIH HHS R01 AI123947NIAID NIH HHS R01 AI129788NIGMS NIH HHS P20 GM103641NIMH NIH HHS R01 MH094755
6 · The paper itself

Abstract

Using a mouse model of multiple sclerosis (MS), experimental autoimmune encephalitis (EAE), we evaluated the role of gut microbiota in modulating chronic-progressive (CP) versus relapse-remitting (RR) forms of the disease. We hypothesized that clinical courses of EAE may be shaped by differential gut microbiota. Metagenomic sequencing of prokaryotic 16S rRNA present in feces from naïve mice and those exhibiting CP-EAE or RR-EAE revealed significantly diverse microbial populations. Microbiota composition was considerably different between naïve strains of mice, suggesting microbial components present in homeostatic conditions may prime mice for divergent courses of disease. Additionally, there were differentially abundant bacteria in CP and RR forms of EAE, indicating a potential role for gut microbiota in shaping tolerant or remittance-favoring, and pathogenic or pro-inflammatory-promoting conditions. Furthermore, immunization to induce EAE led to significant alterations in gut microbiota, some were shared between disease courses and others were course-specific, supporting a role for gut microbial composition in EAE pathogenesis. Moreover, using Linear Discriminant Analysis (LDA) coupled with effect size measurement (LEfSe) to analyze microbial content, biomarkers of each naïve and disease states were identified. Our findings demonstrate for the first time that gut microbiota may determine the susceptibility to CP or RR forms of EAE.

Indexed as

Disease ProgressionGastrointestinal MicrobiomeAnimalsBacillotaChronic DiseaseDisease Models, AnimalDysbiosisFecesFemaleImmunizationMiceMultiple SclerosisRecurrence

Identifiers

PMID31061496
PMCPMC6502871

What OpenQuestion holds

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Registered trials

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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.