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

de novo Crohn’s disease ileal pouch-anal anastomosis pouchitis

Journal

Journal of Crohn's & colitis
ISSN: 1876-4479
Titre abrégé: J Crohns Colitis
Pays: England
ID NLM: 101318676

Informations de publication

Date de publication:
02 Jul 2024
Historique:
received: 05 02 2024
medline: 2 7 2024
pubmed: 2 7 2024
entrez: 2 7 2024
Statut: aheadofprint

Résumé

Biomarkers 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). Uninflamed 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. The 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. Ileal PCP is biologically and clinically relevant in UC and can be used as a biomarker in IBD.

Sections du résumé

BACKGROUND & AIMS OBJECTIVE
Biomarkers 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).
METHODS METHODS
Uninflamed 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.
RESULTS RESULTS
The 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.
CONCLUSIONS CONCLUSIONS
Ileal PCP is biologically and clinically relevant in UC and can be used as a biomarker in IBD.

Identifiants

pubmed: 38953127
pii: 7702486
doi: 10.1093/ecco-jcc/jjae105
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

© The Author(s) 2024. Published by Oxford University Press on behalf of European Crohn’s and Colitis Organisation. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.

Auteurs

Changqing Ma (C)

Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO.

Talin Haritunians (T)

The F. Widjaja Foundation Inflammatory Bowel Disease Institute, Cedars-Sinai Medical Center, Los Angeles, CA.

Anas K Gremida (AK)

Department of Medicine, Washington University School of Medicine, St. Louis, MO.

Gaurav Syal (G)

The F. Widjaja Foundation Inflammatory Bowel Disease Institute, Cedars-Sinai Medical Center, Los Angeles, CA.

Janaki Shah (J)

Department of Medicine, Washington University School of Medicine, St. Louis, MO.

Shaohong Yang (S)

The F. Widjaja Foundation Inflammatory Bowel Disease Institute, Cedars-Sinai Medical Center, Los Angeles, CA.

Claudia Ramos Del Aguila de Rivers (C)

Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA.

Chad E Storer (CE)

Department of Genetics, Washington University School of Medicine, St. Louis, MO.

Ling Chen (L)

Division of Biostatistics, Washington University School of Medicine, St. Louis, MO.

Emebet Mengesha (E)

The F. Widjaja Foundation Inflammatory Bowel Disease Institute, Cedars-Sinai Medical Center, Los Angeles, CA.

Angela Mujukian (A)

The F. Widjaja Foundation Inflammatory Bowel Disease Institute, Cedars-Sinai Medical Center, Los Angeles, CA.

Mary Hanna (M)

The F. Widjaja Foundation Inflammatory Bowel Disease Institute, Cedars-Sinai Medical Center, Los Angeles, CA.

Phillip Fleshner (P)

The F. Widjaja Foundation Inflammatory Bowel Disease Institute, Cedars-Sinai Medical Center, Los Angeles, CA.

David G Binion (DG)

Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA.

Kelli L VanDussen (KL)

Department of Pediatrics, Cincinnati Children's Hospital Medical Center, Cincinnati, OH.

Thaddeus S Stappenbeck (TS)

Department of Inflammation and Immunity, Cleveland Clinic Lerner Research Institute, Cleveland, OH.

Richard D Head (RD)

Department of Genetics, Washington University School of Medicine, St. Louis, MO.

Matthew A Ciorba (MA)

Department of Medicine, Washington University School of Medicine, St. Louis, MO.

Dermot P B McGovern (DPB)

The F. Widjaja Foundation Inflammatory Bowel Disease Institute, Cedars-Sinai Medical Center, Los Angeles, CA.

Ta-Chiang Liu (TC)

Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO.

Classifications MeSH