Evidence map›Paper›PMID 41480237›Full record

ArticleJHEP reports : innovation in hepatology2026

Interleukin-18 binding protein deficiency results in gut microbiota dysbiosis and aggravated diet-induced MASH in mice.

Emmanuel Somm, Elodie Perroud, Yunju Jo, Karina Lindner, Frédérique Ino, Sophie A Montandon, Christelle Veyrat-Durebex, Franck Bontems, Florian Visentin, Nadia Gaïa and 7 more

Abstract read
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In one paragraph

Article in JHEP reports : innovation in hepatology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

17 authors.

Emmanuel SommService of Endocrinology, Diabetes and Metabolism, Department of Medicine, Geneva University Hospitals/University of Geneva, Geneva, Switzerland.
Elodie PerroudService of Endocrinology, Diabetes and Metabolism, Department of Medicine, Geneva University Hospitals/University of Geneva, Geneva, Switzerland.
Yunju JoDepartment of Biomedical Science and Engineering, Gwangju Institute of Science and Technology, Gwangju, South Korea.
Karina LindnerDiabetes Center, Faculty of Medicine, University of Geneva, Geneva, Switzerland.
Frédérique InoService of Endocrinology, Diabetes and Metabolism, Department of Medicine, Geneva University Hospitals/University of Geneva, Geneva, Switzerland.
Sophie A MontandonService of Endocrinology, Diabetes and Metabolism, Department of Medicine, Geneva University Hospitals/University of Geneva, Geneva, Switzerland.
Christelle Veyrat-DurebexDiabetes Center, Faculty of Medicine, University of Geneva, Geneva, Switzerland.
Franck BontemsDiabetes Center, Faculty of Medicine, University of Geneva, Geneva, Switzerland.
Florian VisentinDiabetes Center, Faculty of Medicine, University of Geneva, Geneva, Switzerland.
Nadia GaïaGenomic Research Laboratory, Department of Medicine, Geneva University Hospitals/University of Geneva, Geneva, Switzerland.
Vladimir LazarevicGenomic Research Laboratory, Department of Medicine, Geneva University Hospitals/University of Geneva, Geneva, Switzerland.
Anne-Claude GavinDiabetes Center, Faculty of Medicine, University of Geneva, Geneva, Switzerland.
Jacques SchrenzelGenomic Research Laboratory, Department of Medicine, Geneva University Hospitals/University of Geneva, Geneva, Switzerland.
Dongryeol RyuDepartment of Biomedical Science and Engineering, Gwangju Institute of Science and Technology, Gwangju, South Korea.
Karim GarianiService of Endocrinology, Diabetes and Metabolism, Department of Medicine, Geneva University Hospitals/University of Geneva, Geneva, Switzerland.
Cem GabayDepartment of Pathology and Immunology, Faculty of Medicine, University of Geneva, Geneva, Switzerland.
François R JornayvazService of Endocrinology, Diabetes and Metabolism, Department of Medicine, Geneva University Hospitals/University of Geneva, Geneva, Switzerland.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background & Aims: Metabolic dysfunction-associated steatotic liver disease (MASLD)/metabolic dysfunction-associated steatohepatitis (MASH) are now the most prevalent hepatic disorders worldwide. Growing evidence implicates physiological alterations in the gut-liver axis and gut microbiota dysbiosis in this process. IL-18-binding protein (IL-18BP) forms high affinity complexes with IL-18, thus blocking its interaction with IL-18 receptors. Methods: We used high-fat diet (HFD) and methionine choline deficient (MCD) diet to model MASLD/MASH in wild-type (WT) male mice (n = 6-8 mice per group). We also studied antimicrobial peptides (AMPs) production, gut microbiota composition, and liver phenotype in Results: Feeding WT mice with a HFD or an MCD diet led to a decrease in ileal AMPs expressions (respectively, by 63% and 37% for Conclusions: IL-18BP limits the progression of MASLD/MASH by maintaining normal intestinal production of AMPs and composition of the gut microbiota. Impact and implications: We presently highlight a previously unknown protective role of IL-18BP in the integrity of the gut-liver axis. Increasing IL-18-binding protein levels (a clinically validated option to treat rare systemic auto-inflammatory diseases) represents a novel therapeutic perspective, not only for patients with MASLD/MASH, but also for patients presenting gut microbiota dysbiosis.

Indexed as

FibrosisGut microbiotaInterleukin-18 binding proteinMASHMASLD

Identifiers

PMID41480237
PMCPMC12753522

What Socratic 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 Socratic graph.