Evidence map›Paper›PMID 29637999›Full record

ReviewImmunology2018

Impacts of microbiome metabolites on immune regulation and autoimmunity.

Stefanie Haase, Aiden Haghikia, Nicola Wilck, Dominik N Müller, Ralf A Linker

Open access · bronzeAbstract readReview
In one paragraph

Review in Immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 147 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
147citing papers in PubMed, 4 pooled it
10.0field-weighted citation impact, top 1% 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

147 citing papers in PubMed, 4 syntheses or guidelines pooled it, 236 citations in OpenAlex.

  1. Pooled it
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  5. Review
  6. Article
  7. Is Obesity a Modifiable Risk Factor in Multiple Sclerosis? Mechanistic Insights into Neuroinflammation and Oxidative Damage.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026
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  8. Post-traumatic stress disorder impairs CD8Cell communication and signaling : CCS · 2026
    Article
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  18. Impact of fish consumption on disability progression in multiple sclerosis.Journal of neurology, neurosurgery, and psychiatry · 2025
    Article
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  20. Review

87 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

5 authors at 3 institutions in 1 country.

Stefanie HaaseDepartment of Neurology, Friedrich-Alexander University, Erlangen, Germany.ORCID 0000-0002-9371-4314
Aiden HaghikiaDepartment of Neurology, Ruhr-University Bochum, Bochum, Germany.
Nicola WilckExperimental and Clinical Research Center, a Joint Cooperation of Max-Delbrück Center for Molecular Medicine, Charité-Universitätsmedizin Berlin, Berlin, Germany.
Dominik N MüllerExperimental and Clinical Research Center, a Joint Cooperation of Max-Delbrück Center for Molecular Medicine, Charité-Universitätsmedizin Berlin, Berlin, Germany.
Ralf A LinkerDepartment of Neurology, Friedrich-Alexander University, Erlangen, Germany.
Friedrich-Alexander-Universität Erlangen-Nürnberg · DEMax Delbrück Center · DERuhr University Bochum · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A vast number of studies have demonstrated a remarkable role for the gut microbiota and their metabolites in the pathogenesis of inflammatory diseases, including multiple sclerosis (MS). Recent studies in experimental autoimmune encephalomyelitis, an animal model of MS, have revealed that modifying certain intestinal bacterial populations may influence immune cell priming in the periphery, resulting in dysregulation of immune responses and neuroinflammatory processes in the central nervous system (CNS). Conversely, some commensal bacteria and their antigenic products can protect against inflammation within the CNS. Specific components of the gut microbiome have been implicated in the production of pro-inflammatory cytokines and subsequent generation of Th17 cells. Similarly, commensal bacteria and their metabolites can also promote the generation of regulatory T-cells (Treg), contributing to immune suppression. Short-chain fatty acids may induce Treg either by G-protein-coupled receptors or inhibition of histone deacetylases. Tryptophan metabolites may suppress inflammatory responses by acting on the aryl hydrocarbon receptor in T-cells or astrocytes. Interestingly, secretion of these metabolites can be impaired by excess consumption of dietary components, such as long-chain fatty acids or salt, indicating that the diet represents an environmental factor affecting the complex crosstalk between the gut microbiota and the immune system. This review discusses new aspects of host-microbiota interaction and the immune system with a special focus on MS as a prototype T-cell-mediated autoimmune disease of the CNS.

Indexed as

AutoimmunityEnergy MetabolismImmunomodulationMicrobiotaAnimalsAutoimmune Diseases of the Nervous SystemCentral Nervous SystemDisease SusceptibilityFatty Acids, VolatileGastrointestinal MicrobiomeHumansNeuroimmunomodulationProbioticsTryptophanFatty Acids, VolatileTryptophanexperimental autoimmune encephalomyelitismicrobiome-gut-brain axismultiple sclerosisshort-chain fatty acidsT-cellstryptophan metabolites

Identifiers

PMID29637999
PMCPMC5980218
OpenAlexW2797170123

What OpenQuestion holds

Textmetadata
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.