Evidence map›Paper›PMID 38953127›Full record

ArticleJournal of Crohn's & colitis2024

Ileal Paneth Cell Phenotype is a Cellular Biomarker for Pouch Complications in Ulcerative Colitis.

Changqing Ma, Talin Haritunians, Anas K Gremida, Gaurav Syal, Janaki Shah, Shaohong Yang, Claudia Ramos Del Aguila de Rivers, Chad E Storer, Ling Chen, Emebet Mengesha and 10 more

Abstract read
In one paragraph

Article in Journal of Crohn's & colitis, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Mild Duodenal Mucosal Injury and Increased Type I Interferon Signaling Are Preludes to Celiac Disease.Laboratory investigation; a journal of technical methods and pathology · 2025
    Article
  5. Review
  6. 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

20 authors.

Changqing MaDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO.
Talin HarituniansThe F. Widjaja Foundation Inflammatory Bowel Disease Institute, Cedars-Sinai Medical Center, Los Angeles, CA.ORCID 0000-0002-9005-7750
Anas K GremidaDepartment of Medicine, Washington University School of Medicine, St. Louis, MO.
Gaurav SyalThe F. Widjaja Foundation Inflammatory Bowel Disease Institute, Cedars-Sinai Medical Center, Los Angeles, CA.
Janaki ShahDepartment of Medicine, Washington University School of Medicine, St. Louis, MO.
Shaohong YangThe F. Widjaja Foundation Inflammatory Bowel Disease Institute, Cedars-Sinai Medical Center, Los Angeles, CA.
Claudia Ramos Del Aguila de RiversDepartment of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA.
Chad E StorerDepartment of Genetics, Washington University School of Medicine, St. Louis, MO.
Ling ChenDivision of Biostatistics, Washington University School of Medicine, St. Louis, MO.
Emebet MengeshaThe F. Widjaja Foundation Inflammatory Bowel Disease Institute, Cedars-Sinai Medical Center, Los Angeles, CA.
Angela MujukianThe F. Widjaja Foundation Inflammatory Bowel Disease Institute, Cedars-Sinai Medical Center, Los Angeles, CA.
Mary HannaThe F. Widjaja Foundation Inflammatory Bowel Disease Institute, Cedars-Sinai Medical Center, Los Angeles, CA.
Phillip FleshnerThe F. Widjaja Foundation Inflammatory Bowel Disease Institute, Cedars-Sinai Medical Center, Los Angeles, CA.
David G BinionDepartment of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA.
Kelli L VanDussenDepartment of Pediatrics, Cincinnati Children's Hospital Medical Center, Cincinnati, OH.ORCID 0000-0002-5810-0720
Thaddeus S StappenbeckDepartment of Inflammation and Immunity, Cleveland Clinic Lerner Research Institute, Cleveland, OH.
Richard D HeadDepartment of Genetics, Washington University School of Medicine, St. Louis, MO.
Matthew A CiorbaDepartment of Medicine, Washington University School of Medicine, St. Louis, MO.
Dermot P B McGovernThe F. Widjaja Foundation Inflammatory Bowel Disease Institute, Cedars-Sinai Medical Center, Los Angeles, CA.
Ta-Chiang LiuDepartment of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO.

Funding

Washington University Center for Cellular ImagingP30CA091842 · NCI · WASHINGTON UNIVERSITY · PI TIMOTHY J. EBERLEIN · 2001 to 2026
$128.0M
Washington University DDRCC Supplemental Equipment RequestP30DK052574 · NIDDK · WASHINGTON UNIVERSITY · PI Jeffrey Wade Brown · 2000 to 2026
$30.8M
The Cleveland Digestive Diseases Research Core Center (DDRCC)P30DK097948 · NIDDK · CASE WESTERN RESERVE UNIVERSITY · PI Fabio Cominelli · 2015 to 2026
$15.6M
Utilizing the Phenomics of IBD to Enhance Gene DiscoveryU01DK062413 · NIDDK · CEDARS-SINAI MEDICAL CENTER · PI Dermot Patrick McGovern · 2002 to 2026
$12.2M
Dietary modulation of Paneth cellsR01DK136829 · NIDDK · WASHINGTON UNIVERSITY · PI Ta-Chiang Liu · 2023 to 2026
$2.1M
Paneth cell phenotype as a predictive biomarker for ulcerative colitisR01DK124274 · NIDDK · WASHINGTON UNIVERSITY · PI LIU, TA-CHIANG · 2020 to 2023
$1.5M
Cellular and molecular mechanisms of cigarette smoking-induced Paneth cell abnormalityR01DK125296 · NIDDK · WASHINGTON UNIVERSITY · PI LIU, TA-CHIANG · 2020 to 2023
$1.4M
NCI NIH HHS P30 CA091842NIDDK NIH HHS P30 DK052574NIDDK NIH HHS P30 DK097948NIDDK NIH HHS R01 DK124274NIDDK NIH HHS R01 DK125296NIDDK NIH HHS R01 DK136829NIDDK NIH HHS U01 DK062413
6 · The paper itself

Abstract

BACKGROUND &

aimsBiomarkers that integrate genetic and environmental factors and predict outcome in complex immune diseases such as inflammatory bowel disease (IBD; including Crohn's disease [CD] and ulcerative colitis [UC]) are needed. We showed that morphologic patterns of ileal Paneth cells (Paneth cell phenotype [PCP]; a surrogate for PC function) is one such cellular biomarker for CD. Given the shared features between CD and UC, we hypothesized that PCP is also associated with molecular/genetic features and outcome in UC. Because PC density is highest in the ileum, we further hypothesized that PCP predicts outcome in UC subjects who underwent total colectomy and ileal pouch-anal anastomosis (IPAA).

methodsUninflamed ileal resection margins from UC subjects with colectomy and IPAA were used for PCP and transcriptomic analyses. PCP was defined using defensin 5 immunofluorescence. Genotyping was performed using Immunochip. UC transcriptomic and genotype associations of PCP were incorporated with data from CD subjects to identify common IBD-related pathways and genes that regulate PCP.

resultsThe prevalence of abnormal ileal PCP was 27%, comparable to that seen in CD. Combined analysis of UC and CD subjects showed that abnormal PCP was associated with transcriptomic pathways of secretory granule maturation and polymorphisms in innate immunity genes. Abnormal ileal PCP at the time of colectomy was also associated with pouch complications including de novo CD in the pouch and time to first episode of pouchitis.

conclusionsIleal PCP is biologically and clinically relevant in UC and can be used as a biomarker in IBD.

Indexed as

de novo Crohn’s diseaseileal pouch-anal anastomosispouchitis

Identifiers

PMID38953127
PMCPMC11637519

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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 OpenQuestion graph.