Evidence map›Paper›PMID 32016358›Full record

ArticleJournal of Crohn's & colitis2020

A Pilot Integrative Analysis of Colonic Gene Expression, Gut Microbiota, and Immune Infiltration in Primary Sclerosing Cholangitis-Inflammatory Bowel Disease: Association of Disease With Bile Acid Pathways.

Mohammed Nabil Quraishi, Animesh Acharjee, Andrew D Beggs, Richard Horniblow, Chris Tselepis, Georgios Gkoutos, Subrata Ghosh, A E Rossiter, Nicholas Loman, Willem van Schaik and 4 more

Registry-linked trialOpen access · hybridAbstract read
In one paragraph

Article in Journal of Crohn's & colitis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05376228 (A Systems Biology Approach for Identification of Host and Microbial Mechanisms and Druggable Targets for the Treatment of PSC-IBD), which is not on this map. Cited by 72 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed, 1 pooled it
11.3field-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.

NCT05376228 unknown statusnot on this mapstarted 2022, after this paper: background citation

A Systems Biology Approach for Identification of Host and Microbial Mechanisms and Druggable Targets for the Treatment of PSC-IBD

TypeobservationalSponsorUniversity Hospital Birmingham NHS Foundation TrustRan2022 to 2023Enrolled15ConditionsInflammatory Bowel Diseases, Primary Sclerosing CholangitisArmsOral Vancomycin
3 · Its place in the literature

Who cites it

72 citing papers in PubMed, 1 synthesis or guideline pooled it, 136 citations in OpenAlex.

  1. Pooled it
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  8. Frontiers in microbiology · 2026
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  14. Observational
  15. Liver GPBAR1 Associates With Immune Dysfunction in Primary Sclerosing Cholangitis and Its Activation Attenuates Cholestasis in Abcb4-/- Mice.Liver international : official journal of the International Association for the Study of the Liver · 2025
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12 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

14 authors at 5 institutions in 2 countries.

Mohammed Nabil QuraishiInstitute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, UK.
Animesh AcharjeeInstitute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, UK.
Andrew D BeggsInstitute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, UK.
Richard HorniblowInstitute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, UK.
Chris TselepisInstitute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, UK.
Georgios GkoutosInstitute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, UK.
Subrata GhoshDepartment of Gastroenterology, Queen Elizabeth Hospital, University Hospitals Birmingham, Birmingham, UK.
A E RossiterInstitute of Microbiology and Infection, University of Birmingham, Birmingham, UK.
Nicholas LomanInstitute of Microbiology and Infection, University of Birmingham, Birmingham, UK.
Willem van SchaikInstitute of Microbiology and Infection, University of Birmingham, Birmingham, UK.
David WithersInstitute of Immunology and Immunotherapy, University of Birmingham, Birmingham, UK.
Julian R F WaltersDivision of Digestive Diseases, Imperial College London, London, UK.
Gideon M HirschfieldCentre for Liver and Gastroenterology Research, NIHR Birmingham Biomedical Research Centre, University of Birmingham, Birmingham, UK.
Tariq H IqbalInstitute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, UK.
University of Birmingham · GBQueen Elizabeth Hospital Birmingham · GBImperial College London · GBNIHR Surgical Reconstruction and Microbiology Research Centre · GBUniversity of Toronto · CA

Funding

Department of Health EME/13/179/01Medical Research Council MR/L015080/1Medical Research Council MR/M009157/1Medical Research Council MR/M016587/1Medical Research Council MR/M501621/1Wellcome Trust
6 · The paper itself

Abstract

backgroundAlthough a majority of patients with PSC have colitis [PSC-IBD; primary sclerosing cholangitis-inflammatory bowel disease], this is phenotypically different from ulcerative colitis [UC]. We sought to define further the pathophysiological differences between PSC-IBD and UC, by applying a comparative and integrative approach to colonic gene expression, gut microbiota and immune infiltration data.

methodsColonic biopsies were collected from patients with PSC-IBD [n = 10], UC [n = 10], and healthy controls [HC; n = 10]. Shotgun RNA-sequencing for differentially expressed colonic mucosal genes [DEGs], 16S rRNA analysis for microbial profiling, and immunophenotyping were performed followed by multi-omic integration.

resultsThe colonic transcriptome differed significantly between groups [p = 0.01]. Colonic transcriptomes from HC were different from both UC [1343 DEGs] and PSC-IBD [4312 DEGs]. Of these genes, only 939 had shared differential gene expression in both UC and PSC-IBD compared with HC. Imputed pathways were predominantly associated with upregulation of immune response and microbial defense in both disease cohorts compared with HC. There were 1692 DEGs between PSC-IBD and UC. Bile acid signalling pathways were upregulated in PSC-IBD compared with UC [p = 0.02]. Microbiota profiles were different between the three groups [p = 0.01]; with inferred function in PSC-IBD also being consistent with dysregulation of bile acid metabolism. Th17 cells and IL17-producing CD4 cells were increased in both PSC-IBD and UC when compared with HC [p < 0.05]. Multi-omic integration revealed networks involved in bile acid homeostasis and cancer regulation in PSC-IBD.

conclusionsColonic transcriptomic and microbiota analysis in PSC-IBD point toward dysregulation of colonic bile acid homeostasis compared with UC. This highlights important mechanisms and suggests the possibility of novel approaches in treating PSC-IBD.

Indexed as

Gastrointestinal MicrobiomeTranscriptomeAdultBile Acids and SaltsCase-Control StudiesCholangitis, SclerosingColitis, UlcerativeColonComputational BiologyFemaleHomeostasisHumansImmunityImmunophenotypingInterleukin-17Intestinal MucosaBile Acids and SaltsInterleukin-17RNA, Ribosomal, 16SAutoimmune liver diseasebioinformaticscolitisdysbiosis

Identifiers

PMID32016358
PMCPMC7392170
OpenAlexW3005366639

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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.