Wheat gluten intake increases the severity of experimental colitis and bacterial translocation by weakening of the proteins of the junctional complex

Gluten is only partially digested by intestinal enzymes and can generate peptides that can alter intestinal permeability, facilitating bacterial translocation, thus affecting the immune system. Few studies addressed the role of diet with gluten in the development of colitis. Therefore, we investigat...

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Published in:	British journal of nutrition Vol. 121; no. 4; pp. 361 - 373
Main Authors:	Menta, Penélope L. R., Andrade, Maria E. R., Leocádio, Paola C. L., Fraga, Júlia R., Dias, Melissa T. S., Cara, Denise C., Cardoso, Valbert N., Borges, Luciano F., Capettini, Luciano S. A., Aguilar, Edenil C., Alvarez-Leite, Jacqueline I.
Format:	Journal Article
Language:	English
Published:	Cambridge, UK Cambridge University Press 28-02-2019
Subjects:	Adaptation Adhesion Animals Bacteria Bacterial Translocation - immunology Celiac disease Colitis Colitis - chemically induced Colitis - immunology Colitis - microbiology Colon Desmosomes Dextran Dextran Sulfate Diet Diet - adverse effects Disease Models, Animal E-cadherin Enzymes Female Gastrointestinal Microbiome - immunology Gluten Glutens - adverse effects Immune system Inflammation Inflammatory bowel disease Intestinal Mucosa - immunology Intestine Membrane permeability Mice Mice, Inbred C57BL Migration Molecular Nutrition Mucosa Organs Peptides Permeability Proteins Rodents Sodium Structural damage Tight Junctions - immunology Translocation Triticum - chemistry Vacuoles Wheat β-Catenin Asia Europe Experimental colitis Gluten Bacterial translocation Intestinal permeability Col + G colitis + gluten 99mTc 99mtechnetium DSS sodium dextran sulphate C control TEM transmission electron microscopy ATI amylase–trypsin inhibitor Col colitis UC ulcerative colitis IBD inflammatory bowel disease
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Summary:	Gluten is only partially digested by intestinal enzymes and can generate peptides that can alter intestinal permeability, facilitating bacterial translocation, thus affecting the immune system. Few studies addressed the role of diet with gluten in the development of colitis. Therefore, we investigate the effects of wheat gluten-containing diet on the evolution of sodium dextran sulphate (DSS)-induced colitis. Mice were fed a standard diet without (colitis group) or with 4·5 % wheat gluten (colitis + gluten) for 15 d and received DSS solution (1·5 %, w/v) instead of water during the last 7 d. Compared with the colitis group, colitis + gluten mice presented a worse clinical score, a larger extension of colonic injury area, and increased mucosal inflammation. Both intestinal permeability and bacterial translocation were increased, propitiating bacteria migration for peripheral organs. The mechanism by which diet with gluten exacerbates colitis appears to be related to changes in protein production and organisation in adhesion junctions and desmosomes. The protein α-E-catenin was especially reduced in mice fed gluten, which compromised the localisation of E-cadherin and β-catenin proteins, weakening the structure of desmosomes. The epithelial damage caused by gluten included shortening of microvilli, a high number of digestive vacuoles, and changes in the endosome/lysosome system. In conclusion, our results show that wheat gluten-containing diet exacerbates the mucosal damage caused by colitis, reducing intestinal barrier function and increasing bacterial translocation. These effects are related to the induction of weakness and disorganisation of adhesion junctions and desmosomes as well as shortening of microvilli and modification of the endocytic vesicle route.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	0007-1145 1475-2662
DOI:	10.1017/S0007114518003422