Evidence map›Paper›PMID 41766816›Full record

ArticleFrontiers in immunology2025

The gut microbiota composition is shaped by disease activity and individual treatment responses in patients with multiple sclerosis.

Veronika Ticha, Stepan Coufal, Zuzana Jiraskova Zakostelska, Tomas Thon, Radka Roubalova, Tomas Hrncir, Miloslav Kverka, Miluse Pavelcova, Pavlina Kleinova, Jana Lizrova Preiningerova and 4 more

Abstract read
In one paragraph

Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–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

2 citing papers in PubMed.

  1. Significant changes in the fecal bacteriobiota richness and diversity in patients with relapsing-remitting multiple sclerosis compared to healthy individuals.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2026
    Article
  2. Review
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

14 authors.

Veronika Ticha *Department of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University and General University Hospital in Prague, Prague, Czechia.
Stepan Coufal *Laboratory of Cellular and Molecular Immunology, Institute of Microbiology of the Czech Academy of Sciences, Prague, Czechia.
Zuzana Jiraskova ZakostelskaLaboratory of Cellular and Molecular Immunology, Institute of Microbiology of the Czech Academy of Sciences, Prague, Czechia.
Tomas ThonLaboratory of Cellular and Molecular Immunology, Institute of Microbiology of the Czech Academy of Sciences, Prague, Czechia.
Radka RoubalovaLaboratory of Cellular and Molecular Immunology, Institute of Microbiology of the Czech Academy of Sciences, Prague, Czechia.
Tomas HrncirLaboratory of Gnotobiology, Institute of Microbiology of the Czech Academy of Sciences, Novy Hradek, Czechia.
Miloslav KverkaLaboratory of Cellular and Molecular Immunology, Institute of Microbiology of the Czech Academy of Sciences, Prague, Czechia.
Miluse PavelcovaDepartment of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University and General University Hospital in Prague, Prague, Czechia.
Pavlina KleinovaDepartment of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University and General University Hospital in Prague, Prague, Czechia.
Jana Lizrova PreiningerovaDepartment of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University and General University Hospital in Prague, Prague, Czechia.
Ivana KovarovaDepartment of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University and General University Hospital in Prague, Prague, Czechia.
Jakub KreisingerLaboratory of Animal Evolutionary Biology, Faculty of Science, Department of Zoology, Charles University, Prague, Czechia.
Helena Tlaskalova-HogenovaLaboratory of Cellular and Molecular Immunology, Institute of Microbiology of the Czech Academy of Sciences, Prague, Czechia.
Eva Kubala HavrdovaDepartment of Neurology and Centre of Clinical Neuroscience, First Faculty of Medicine, Charles University and General University Hospital in Prague, Prague, Czechia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple sclerosis (MS) is a chronic autoimmune disorder of the central nervous system, with both animal and human studies highlighting a pivotal role for the gut microbiota in its pathogenesis. In this cross-sectional study, we investigated the potential role of gut microbiota in treatment response by analyzing its composition using 16S rRNA sequencing in treatment-naïve patients and those receiving disease-modifying therapies (interferon-beta (IFN-β), fingolimod, or cladribine), compared to healthy controls (HC). We also analyzed differences in gut microbiota composition and the serum levels of biomarkers associated with microbial translocation and inflammation based on treatment response. We found that individuals with clinically isolated syndrome (CIS) and treatment non-responders (NR) had significantly different alpha and beta diversity compared to HC. This effect was present in both IFN-β and fingolimod treatment. Individuals treated with cladribine had significantly different alpha and beta diversity regardless of the treatment outcome. The main differences in abundances in CIS and NR were found in bacteria that produce short-chain fatty acids. These patients also had significantly higher levels of lipopolysaccharide-binding protein and mannose-binding lectin compared to HC suggesting the compromised gut barrier function in multiple sclerosis leading to higher level of microbial translocation in these patients. In summary, we found that the treatment influences gut microbiota. Similar profile of gut microbiota and higher levels of molecules associated with microbial translocation were observed in patients with active disease (CIS and NR), suggesting the higher permeability of their gut barrier leading to pro-inflammatory tunning of their immune system.

Indexed as

Gastrointestinal MicrobiomeMultiple SclerosisAdultBiomarkersCladribineCross-Sectional StudiesFemaleFingolimod HydrochlorideHumansImmunosuppressive AgentsInterferon-betaMaleMiddle AgedRNA, Ribosomal, 16STreatment OutcomeBiomarkersCladribineFingolimod HydrochlorideImmunosuppressive AgentsInterferon-betaRNA, Ribosomal, 16Scladribinedisease modifying therapiesfingolimodinterferon-βmultiple sclerosisneuroinflammationserum biomarkers

Identifiers

PMID41766816
PMCPMC12935932

What Socratic holds

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LicenceCC BY
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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 Socratic graph.