Evidence map›Paper›PMID 33899089›Full record

Trial reportBrain : a journal of neurology2021

Dietary conjugated linoleic acid links reduced intestinal inflammation to amelioration of CNS autoimmunity.

Ann-Katrin Fleck, Stephanie Hucke, Flavio Teipel, Melanie Eschborn, Claudia Janoschka, Marie Liebmann, Haleluya Wami, Lisanne Korn, Geethanjali Pickert, Marvin Hartwig and 13 more

Open access · bronzeAbstract readClinical Trial
In one paragraph

Trial report in Brain : a journal of neurology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

28 citing papers in PubMed, 46 citations in OpenAlex.

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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

23 authors at 4 institutions in 2 countries.

Ann-Katrin FleckDepartment of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany.
Stephanie HuckeDepartment of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany.
Flavio TeipelDepartment of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany.ORCID 0000-0002-0233-9732
Melanie EschbornDepartment of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany.
Claudia JanoschkaDepartment of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany.
Marie LiebmannDepartment of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany.
Haleluya WamiInstitute for Hygiene, University Hospital Münster, Münster, Germany.
Lisanne KornDepartment of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany.
Geethanjali PickertInstitute of Translational Immunology, University Medical Center Mainz, Mainz, Germany.
Marvin HartwigDepartment of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany.
Timo WirthDepartment of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany.
Martin HeroldDepartment of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany.
Kathrin KochDepartment of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany.
Maren Falk-PaulsenInstitute of Clinical Molecular Biology, University of Kiel, Kiel, Germany.
Ulrich DobrindtInstitute for Hygiene, University Hospital Münster, Münster, Germany.
Stjepana KovacDepartment of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany.
Catharina C GrossDepartment of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany.
Philip RosenstielInstitute of Clinical Molecular Biology, University of Kiel, Kiel, Germany.
Marcel TrautmannDivision of Translational Pathology, Gerhard-Domagk-Institute of Pathology, University Hospital Münster, Münster, Germany.ORCID 0000-0002-5842-1196
Heinz WiendlDepartment of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany.
Detlef SchuppanInstitute of Translational Immunology, University Medical Center Mainz, Mainz, Germany.
Tanja KuhlmannDepartment of Neuropathology, University of Münster, Münster, Germany.
Luisa KlotzDepartment of Neurology with Institute of Translational Neurology, University Hospital Münster, Münster, Germany.
University Hospital Münster · DEBeth Israel Deaconess Medical Center · USJohannes Gutenberg University Mainz · DEUniversity of Münster · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A close interaction between gut immune responses and distant organ-specific autoimmunity including the CNS in multiple sclerosis has been established in recent years. This so-called gut-CNS axis can be shaped by dietary factors, either directly or via indirect modulation of the gut microbiome and its metabolites. Here, we report that dietary supplementation with conjugated linoleic acid, a mixture of linoleic acid isomers, ameliorates CNS autoimmunity in a spontaneous mouse model of multiple sclerosis, accompanied by an attenuation of intestinal barrier dysfunction and inflammation as well as an increase in intestinal myeloid-derived suppressor-like cells. Protective effects of dietary supplementation with conjugated linoleic acid were not abrogated upon microbiota eradication, indicating that the microbiome is dispensable for these conjugated linoleic acid-mediated effects. Instead, we observed a range of direct anti-inflammatory effects of conjugated linoleic acid on murine myeloid cells including an enhanced IL10 production and the capacity to suppress T-cell proliferation. Finally, in a human pilot study in patients with multiple sclerosis (n = 15, under first-line disease-modifying treatment), dietary conjugated linoleic acid-supplementation for 6 months significantly enhanced the anti-inflammatory profiles as well as functional signatures of circulating myeloid cells. Together, our results identify conjugated linoleic acid as a potent modulator of the gut-CNS axis by targeting myeloid cells in the intestine, which in turn control encephalitogenic T-cell responses.

Indexed as

Dietary SupplementsAdultAnimalsAutoimmunityEncephalomyelitis, Autoimmune, ExperimentalEnteritisFemaleHumansLinoleic Acids, ConjugatedMaleMiceMice, Inbred C57BLMonocytesMultiple Sclerosis, Relapsing-RemittingPilot ProjectsProof of Concept StudyLinoleic Acids, Conjugatedconjugated linoleic aciddietary supplementationgut–CNS axisintestinal inflammationmultiple sclerosis

Identifiers

PMID33899089
PMCPMC8105041
OpenAlexW3158889839

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.