Wheat Consumption Aggravates Colitis in Mice via Amylase Trypsin Inhibitor-mediated Dysbiosis.
Animal Feed
/ adverse effects
Animals
Colitis
/ chemically induced
Dextran Sulfate
/ toxicity
Disease Models, Animal
Dysbiosis
/ complications
Fecal Microbiota Transplantation
Feces
/ microbiology
Gastrointestinal Microbiome
/ immunology
Humans
Immunity, Innate
Inflammatory Bowel Diseases
/ chemically induced
Male
Mice
Mice, Knockout
Plant Proteins, Dietary
/ adverse effects
Severity of Illness Index
Signal Transduction
/ genetics
Toll-Like Receptor 4
/ genetics
Triticum
/ immunology
Trypsin Inhibitors
/ adverse effects
Inflammatory bowel diseases
microbiome
mouse model
wheat sensitivity
Journal
Gastroenterology
ISSN: 1528-0012
Titre abrégé: Gastroenterology
Pays: United States
ID NLM: 0374630
Informations de publication
Date de publication:
07 2020
07 2020
Historique:
received:
28
08
2018
revised:
06
03
2020
accepted:
26
03
2020
pubmed:
7
4
2020
medline:
1
4
2021
entrez:
7
4
2020
Statut:
ppublish
Résumé
Wheat has become the world's major staple and its consumption correlates with prevalence of noncommunicable disorders such as inflammatory bowel diseases. Amylase trypsin inhibitors (ATIs), a component of wheat, activate the intestine's innate immune response via toll-like receptor 4 (TLR4). We investigated the effects of wheat and ATIs on severity of colitis and fecal microbiota in mice. C57BL/6 wild-type and Tlr4 The wheat- or ATI-containing diets equally increased inflammation in intestinal tissues of C57BL/6 mice with colitis, compared with mice on control diets. The ATI-containing diet promoted expansion of taxa associated with development of colitis comparable to the wheat-containing diet. ATIs inhibited proliferation of specific human commensal bacteria in radial diffusion assays. Transplantation of microbiota from feces of mice fed the wheat- or ATI-containing diets to intestines of mice on control diets increased the severity of colitis in these mice. The ATI-containing diet did not increase the severity of colitis in Tlr4 Consumption of wheat or wheat ATIs increases intestinal inflammation in mice with colitis, via TLR4, and alters their fecal microbiota. Wheat-based, ATI-containing diets therefore activate TLR4 signaling and promote intestinal dysbiosis.
Sections du résumé
BACKGROUND & AIMS
Wheat has become the world's major staple and its consumption correlates with prevalence of noncommunicable disorders such as inflammatory bowel diseases. Amylase trypsin inhibitors (ATIs), a component of wheat, activate the intestine's innate immune response via toll-like receptor 4 (TLR4). We investigated the effects of wheat and ATIs on severity of colitis and fecal microbiota in mice.
METHODS
C57BL/6 wild-type and Tlr4
RESULTS
The wheat- or ATI-containing diets equally increased inflammation in intestinal tissues of C57BL/6 mice with colitis, compared with mice on control diets. The ATI-containing diet promoted expansion of taxa associated with development of colitis comparable to the wheat-containing diet. ATIs inhibited proliferation of specific human commensal bacteria in radial diffusion assays. Transplantation of microbiota from feces of mice fed the wheat- or ATI-containing diets to intestines of mice on control diets increased the severity of colitis in these mice. The ATI-containing diet did not increase the severity of colitis in Tlr4
CONCLUSIONS
Consumption of wheat or wheat ATIs increases intestinal inflammation in mice with colitis, via TLR4, and alters their fecal microbiota. Wheat-based, ATI-containing diets therefore activate TLR4 signaling and promote intestinal dysbiosis.
Identifiants
pubmed: 32251667
pii: S0016-5085(20)30447-9
doi: 10.1053/j.gastro.2020.03.064
pii:
doi:
Substances chimiques
Plant Proteins, Dietary
0
Tlr4 protein, mouse
0
Toll-Like Receptor 4
0
Trypsin Inhibitors
0
Dextran Sulfate
9042-14-2
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
257-272.e17Informations de copyright
Copyright © 2020 AGA Institute. Published by Elsevier Inc. All rights reserved.