Evidence map›Paper›PMID 32745639›Full record

Trial reportCellular and molecular gastroenterology and hepatology2021

Genome-Wide Transcriptomic Analysis of Intestinal Mucosa in Celiac Disease Patients on a Gluten-Free Diet and Postgluten Challenge.

Valeriia Dotsenko, Mikko Oittinen, Juha Taavela, Alina Popp, Markku Peräaho, Synnöve Staff, Jani Sarin, Francisco Leon, Jorma Isola, Markku Mäki and 1 more

Registry-linked trialOpen access · goldAbstract readClinical Trial, Phase IIRandomized Controlled Trial
In one paragraph

Trial report in Cellular and molecular gastroenterology and hepatology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07556328 (Histological and Molecular Profiling in the Diagnostics and Treatment of Small-Bowel Diseases - A Prospective Cohort Study), which is not on this map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
8.0field-weighted citation impact, top 2% 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.

NCT07556328 recruitingnot on this mapstarted 2025, after this paper: background citation

Histological and Molecular Profiling in the Diagnostics and Treatment of Small-Bowel Diseases - A Prospective Cohort Study (The DeepBowel Study)

Typeobservational_patient_registrySponsorTampere University HospitalRan2025 to 2035Enrolled300ConditionsCeliac Disease, Small Bowel Disease, Refractory Celiac Disease
3 · Its place in the literature

Who cites it

46 citing papers in PubMed, 72 citations in OpenAlex.

  1. Trial
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  5. Gliadin-specific CD4Science advances · 2026
    Article
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  11. IFN-γ is a direct driver of crypt hyperplasia in celiac disease.The Journal of clinical investigation · 2025
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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

11 authors at 5 institutions in 3 countries.

Valeriia DotsenkoTampere Center for Child Health Research, Faculty of Medicine and Health Technology, Tampere University Hospital, Tampere University Tampere, Finland.
Mikko OittinenTampere Center for Child Health Research, Faculty of Medicine and Health Technology, Tampere University Hospital, Tampere University Tampere, Finland.
Juha TaavelaTampere Center for Child Health Research, Faculty of Medicine and Health Technology, Tampere University Hospital, Tampere University Tampere, Finland; Department of Internal Medicine, Central Finland Central Hospital, Jyväskylä, Finland.
Alina PoppTampere Center for Child Health Research, Faculty of Medicine and Health Technology, Tampere University Hospital, Tampere University Tampere, Finland; Pediatric Department, Carol Davila University of Medicine and Pharmacy, Alessandrescu-Rusescu National Institute for Mother and Child Health, Bucharest, Romania.
Markku PeräahoDepartment of Internal Medicine, Central Finland Central Hospital, Jyväskylä, Finland.
Synnöve StaffDepartment of Obstetrics and Gynecology and Tays Cancer Centre, Faculty of Medicine and Health Technology, Tampere University Hospital, Tampere University, Tampere, Finland.
Jani SarinLaboratory of Cancer Biology, Faculty of Medicine and Health Technology, Tampere University, Tampere, Finland; Jilab Inc, Tampere, Finland.
Francisco LeonCelimmune LLC, Bethesda, Maryland.
Jorma IsolaLaboratory of Cancer Biology, Faculty of Medicine and Health Technology, Tampere University, Tampere, Finland; Jilab Inc, Tampere, Finland.
Markku MäkiTampere Center for Child Health Research, Faculty of Medicine and Health Technology, Tampere University Hospital, Tampere University Tampere, Finland.
Keijo ViiriTampere Center for Child Health Research, Faculty of Medicine and Health Technology, Tampere University Hospital, Tampere University Tampere, Finland. Electronic address: keijo.viiri@tuni.fi.
Tampere University Hospital · FITampere University of Applied Sciences · FICarol Davila University of Medicine and Pharmacy · ROCelimmune (United States) · USCentral Finland Health Care District · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND &

aimsGluten challenge studies are instrumental in understanding the pathophysiology of celiac disease. Our aims in this study were to reveal early gluten-induced transcriptomic changes in duodenal biopsies and to find tools for clinics.

methodsDuodenal biopsies were collected from 15 celiac disease patients on a strict long-term gluten-free diet (GFD) prior to and post a gluten challenge (PGC) and from 6 healthy control individuals (DC). Biopsy RNA was subjected to genome-wide 3' RNA-Seq. Sequencing data was used to determine the differences between the three groups and was compared to sequencing data from the public repositories. The biopsies underwent morphometric analyses.

resultsIn DC vs. GFD group comparisons, 167 differentially expressed genes were identified with 117 genes downregulated and 50 genes upregulated. In PGC vs. GFD group comparisons, 417 differentially expressed genes were identified with 195 genes downregulated and 222 genes upregulated. Celiac disease patients on a GFD were not "healthy". In particular, genes encoding proteins for transporting small molecules were expressed less. In addition to the activation of immune response genes, a gluten challenge induced hyperactive intestinal wnt-signaling and consequent immature crypt gene expression resulting in less differentiated epithelium. Biopsy gene expression in response to a gluten challenge correlated with the extent of the histological damage. Regression models using only four gene transcripts described 97.2% of the mucosal morphology and 98.0% of the inflammatory changes observed.

conclusionsOur gluten challenge trial design provided an opportunity to study the transition from health to disease. The results show that even on a strict GFD, despite being deemed healthy, patients reveal patterns of ongoing disease. Here, a transcriptomic regression model estimating the extent of gluten-induced duodenal mucosal injury is presented.

Indexed as

AdultBiopsyCeliac DiseaseDatasets as TopicDiet, Gluten-FreeDuodenumFemaleGlutensHumansIntestinal MucosaMaleMiddle AgedRNA-SeqTranscriptomeYoung AdultGlutensCeliac DiseaseGluten ChallengeGluten-Free DietMorphometryRNA-Seq

Identifiers

PMID32745639
PMCPMC7593586
OpenAlexW3046905536

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

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 Socratic graph.