Ileocolonic Histopathological and Microbial Alterations in the Irritable Bowel Syndrome: A Nested Community Case-Control Study.


Journal

Clinical and translational gastroenterology
ISSN: 2155-384X
Titre abrégé: Clin Transl Gastroenterol
Pays: United States
ID NLM: 101532142

Informations de publication

Date de publication:
22 12 2020
Historique:
received: 27 07 2020
accepted: 23 11 2020
entrez: 19 1 2021
pubmed: 20 1 2021
medline: 9 9 2021
Statut: epublish

Résumé

Histopathological alterations in the ileum and colon in irritable bowel syndrome (IBS) are controversial, and normal values are poorly established. We hypothesized that changes in mucosal immune cells characterize IBS and key changes in immune composition are associated with the mucosa-associated microbiota (MaM). A nested case-control study (48 IBS and 106 controls included) from 745 colonoscopy participants in a random population sample. Intraepithelial lymphocytes (IELs)/100 enterocytes and eosinophils/5 nonoverlapping high-power fields counted; mast cells identified by immunocytochemistry (CD117)/5 high-power fields. Paneth cells quantified per 5 crypts. 16S rRNA gene amplicon sequencing performed on available sigmoid MaM, n = 55 and fecal microbiota, n = 20. Microbiota profiles compared between samples with high and low IEL counts. IBS had increased IELs in the terminal ileum (relative risk ratio = 1.70, 95% confidence interval 1.08-2.76, P = 0.022 adjusted for age, sex, and smoking). Cecal IELs were increased in IBS-diarrhea (relative risk ratio = 2.03, 95% confidence interval 1.13-3.63, P = 0.017). No difference was observed in alpha diversity of MaM or fecal microbiota based on IEL count. There was no difference in beta diversity of the MaM according to IEL count in the terminal ileal (TI) (P = 0.079). High TI IEL counts associated with a significant expansion of the genus Blautia (P = 0.024) and unclassified Clostridiales (P = 0.036) in colon MaM. A modest but significant increase in IELs was observed in IBS vs. controls in a population-based setting. Subtle TI and cecal inflammation may play a pathogenic role in IBS but needs confirmation. Modest but discernible differences in the colonic MaM were seen according to TI IEL count but not IBS status.

Identifiants

pubmed: 33464728
doi: 10.14309/ctg.0000000000000296
pii: 01720094-202101000-00010
pmc: PMC8345925
doi:

Substances chimiques

DNA, Bacterial 0
RNA, Ribosomal, 16S 0

Types de publication

Journal Article Observational Study Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

e00296

Informations de copyright

Copyright © 2020 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of The American College of Gastroenterology.

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Auteurs

Nicholas J Talley (NJ)

Faculty of Health and Medicine, University of Newcastle, Newcastle, Australia.
NHMRC Center of Research Excellence in Digestive Health Newcastle, Australia.

James L Alexander (JL)

Division of Digestive Disease, Imperial College London, London, UK.

Marjorie M Walker (MM)

NHMRC Center of Research Excellence in Digestive Health Newcastle, Australia.
Department of Anatomical Pathology, University of Newcastle, Newcastle, Australia.

Michael P Jones (MP)

NHMRC Center of Research Excellence in Digestive Health Newcastle, Australia.
Department of Psychology, Macquarie University, North Ryde, Australia.

Luisa W Hugerth (LW)

Center for Translational Microbiome Research, CTMR, Department of Microbiology, Tumor and Cell Biology (MTC), Karolinska Institutet, Science for Life Laboratory, Solna, Sweden.

Lars Engstrand (L)

Center for Translational Microbiome Research, CTMR, Department of Microbiology, Tumor and Cell Biology (MTC), Karolinska Institutet, Science for Life Laboratory, Solna, Sweden.

Lars Agréus (L)

Division for Family Medicine and Primary Care, Karolinska Institutet, Huddinge, Sweden.

Nicholas Powell (N)

NHMRC Center of Research Excellence in Digestive Health Newcastle, Australia.
Division of Digestive Disease, Imperial College London, London, UK.

Anna Andreasson (A)

Department of Psychology, Macquarie University, North Ryde, Australia.
Stress Research Institute, Stockholm University, Stockholm, Sweden.
Department of Medicine Solna, Karolinska Institutet, Solna, Sweden.

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Classifications MeSH