Evidence map›Paper›PMID 38358371›Full record

ArticleHepatology communications2024

Increased type-I interferon level is associated with liver damage and fibrosis in primary sclerosing cholangitis.

Rebekka J S Salzmann, Christina Krötz, Tudor Mocan, Lavinia P Mocan, Cristiana Grapa, Sophia Rottmann, Ramona Reichelt, Cindy M Keller, Bettina Langhans, Frederik Schünemann and 14 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
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Article in Hepatology communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.7field-weighted citation impact, top 32% 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

0 citing papers in PubMed, 2 citations in OpenAlex.

No citing paper in PubMed yet.

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

24 authors at 8 institutions in 3 countries.

Rebekka J S SalzmannDepartment of Immunodynamic, Institute of Molecular Medicine and Experimental Immunology, University Hospital Bonn of the Rheinische Friedrich-Wilhelms-University, Bonn, Germany.
Christina KrötzDepartment of Medicine II, Saarland University Medical Center, Homburg, Germany.
Tudor MocanUBBMed Department, Babes-Bolyai University, Cluj-Napoca, Romania.
Lavinia P MocanDepartment of Histology, Iuliu Haţieganu University of Medicine and Pharmacy, Cluj-Napoca, Romania.
Cristiana GrapaDepartment of Physiology, Iuliu Haţieganu University of Medicine and Pharmacy, Cluj-Napoca, Romania.
Sophia RottmannDepartment of Immunodynamic, Institute of Molecular Medicine and Experimental Immunology, University Hospital Bonn of the Rheinische Friedrich-Wilhelms-University, Bonn, Germany.
Ramona ReicheltDepartment of Immunodynamic, Institute of Molecular Medicine and Experimental Immunology, University Hospital Bonn of the Rheinische Friedrich-Wilhelms-University, Bonn, Germany.
Cindy M KellerDepartment of Immunodynamic, Institute of Molecular Medicine and Experimental Immunology, University Hospital Bonn of the Rheinische Friedrich-Wilhelms-University, Bonn, Germany.
Bettina LanghansDepartment of Internal Medicine I, University Hospital Bonn of the Rheinische Friedrich-Wilhelms-University, Bonn, Germany.
Frederik SchünemannDepartment for Biosciences of Sports, Institute of Sport Science, University of Hildesheim, Hildesheim, Germany.
Alexander PohlDepartment for Biosciences of Sports, Institute of Sport Science, University of Hildesheim, Hildesheim, Germany.
Thomas BöhlerDepartment for Biosciences of Sports, Institute of Sport Science, University of Hildesheim, Hildesheim, Germany.
Käthe BersinerDepartment for Biosciences of Sports, Institute of Sport Science, University of Hildesheim, Hildesheim, Germany.
Marcin KrawczykDepartment of Medicine II, Saarland University Medical Center, Homburg, Germany.
Piotr MilkiewiczLaboratory of Metabolic Liver Diseases, Department of General, Transplant and Liver Surgery, Centre for Preclinical Research, Medical University of Warsaw, Warsaw, Poland.
Zeno Sparchez3rd Medical Department, Iuliu Haţieganu University of Medicine and Pharmacy, Cluj-Napoca, Romania.
Frank LammertHannover Medical School (MHH), Hannover, Germany.
Sebastian GehlertDepartment for Biosciences of Sports, Institute of Sport Science, University of Hildesheim, Hildesheim, Germany.
Maria A Gonzalez-CarmonaDepartment of Internal Medicine I, University Hospital Bonn of the Rheinische Friedrich-Wilhelms-University, Bonn, Germany.
Arnulf WillmsDepartment of General, Visceral and Thoracic Surgery, German Armed Forces Central Hospital, Koblenz, Germany.
Christian P StrassburgDepartment of Internal Medicine I, University Hospital Bonn of the Rheinische Friedrich-Wilhelms-University, Bonn, Germany.
Miroslaw T KornekDepartment of Internal Medicine I, University Hospital Bonn of the Rheinische Friedrich-Wilhelms-University, Bonn, Germany.
Leona DoldDepartment of Internal Medicine I, University Hospital Bonn of the Rheinische Friedrich-Wilhelms-University, Bonn, Germany.
Veronika Lukacs-KornekDepartment of Immunodynamic, Institute of Molecular Medicine and Experimental Immunology, University Hospital Bonn of the Rheinische Friedrich-Wilhelms-University, Bonn, Germany.
University Hospital Bonn · DEUniversity of Hildesheim · DEIuliu Hațieganu University of Medicine and Pharmacy · ROMedical University of Warsaw · PLBundeswehrBundeswehrzentralkrankenhaus Koblenz · DEMedizinische Hochschule Hannover · DESaarland University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe level of type-I interferons (IFNs) in primary sclerosing cholangitis (PSC) was investigated to evaluate its association with disease activity and progression.

methodsBioactive type-I IFNs were evaluated in a murine model of PSC and human patients' sera using a cell-based reporter assay and ELISA techniques. In total, 57 healthy participants, 71 PSC, and 38 patients with primary biliary cholangitis were enrolled in this study.

resultsBioactive type-I IFNs were elevated in the liver and serum of multidrug resistance protein 2-deficient animals and showed a correlation with the presence of CD45+ immune cells and serum alanine transaminase levels. Concordantly, bioactive type-I IFNs were elevated in the sera of patients with PSC as compared to healthy controls (sensitivity of 84.51%, specificity of 63.16%, and AUROC value of 0.8267). Bioactive IFNs highly correlated with alkaline phosphatase (r=0.4179, p<0.001), alanine transaminase (r=0.4704, p<0.0001), and gamma-glutamyl transpeptidase activities (r=0.6629, p<0.0001) but not with serum bilirubin. In addition, patients with PSC with advanced fibrosis demonstrated significantly higher type-I IFN values. Among the type-I IFN subtypes IFNα, β and IFNω could be detected in patients with PSC with IFNω showing the highest concentration among the subtypes and being the most abundant among patients with PSC.

conclusionsThe selectively elevated bioactive type-I IFNs specifically the dominating IFNω could suggest a novel inflammatory pathway that might also have a hitherto unrecognized role in the pathomechanism of PSC.

Indexed as

Cholangitis, SclerosingInterferon Type ILiverAlanine TransaminaseAnimalsFibrosisHumansMiceAlanine TransaminaseInterferon Type I

Identifiers

PMID38358371
PMCPMC10871749
OpenAlexW4391839943

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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.