Grant: Operating Grant
McMaster University
$648,752.00
The role of human intestinal microbiota in dietary gluten metabolism and inflammation
EF 2014-15
Résumé
Gluten-related disorders (GRD) include all diseases triggered by dietary gluten. The best characterized condition is celiac disease, a severe inflammation of the small intestine. The only current treatment for celiac disease is a strict gluten-free diet, which has some limitations, as this is a restrictive and expensive diet. An increasing number of people are sensitive to gluten with one in 100 Canadians suffering from celiac disease. The reason for the increase in inflammatory and symptomatic reactions to gluten is unclear, but may relate to changes in dietary and hygiene habits that affect the bacteria that normally inhabit our gut. One of the main problems with gluten is that it consists of proteins that are difficult to break down by our digestive enzymes. Gut bacteria are armed with a variety of enzymes and can completely or incompletely digest gluten. Complete degradation of gluten would be beneficial, but incomplete degradation by gut bacteria may increase the chances to develop celiac disease. In this proposal I will explore the role of gut bacteria isolated from patients with celiac disease and non celiac people in the digestion of dietary gluten and in the modulation of inflammation produced by this common protein in our diet. I propose that the bacteria that inhabit the gut of celiac patients have impaired capacity to digest gluten and that their enzymes produce toxic peptides from gluten that contribute to inflammation. Thus, celiac disease may be prevented, or better treated, by inhibiting these bacteria or their products.
Programme
Operating Grant
Bénéficiaire
Emplacement
Ontario, Canada
Type de bénéficiaire
Academia
Type
Grant
Source
CIHR Funding Decisions Database
Tel que publié
Id
320659
Name
Verdu Elena F
Region
Ontario
Country
Canada
Orgtype
Institution Paid; Research Institution
Instname2
Nutrition, Metabolism and Diabetes
Theme2
Biomedical
Prcname2
Nutrition, Food & Health
Projecttitle
The role of human intestinal microbiota in dietary gluten metabolism and inflammation
Programtype2
Operating Grants
Orgnameinp2
McMaster University
Cihramount2
$648,752
Cihrequipment2
$0
Programname2
Operating Grant
Keyworddelim
Celiac Disease; Gluten Sensitivity; Intestinal Microbiota; Probiotics
Abstract
Gluten-related disorders (GRD) include all diseases triggered by dietary gluten. The best characterized condition is celiac disease, a severe inflammation of the small intestine. The only current treatment for celiac disease is a strict gluten-free diet, which has some limitations, as this is a restrictive and expensive diet. An increasing number of people are sensitive to gluten with one in 100 Canadians suffering from celiac disease. The reason for the increase in inflammatory and symptomatic reactions to gluten is unclear, but may relate to changes in dietary and hygiene habits that affect the bacteria that normally inhabit our gut. One of the main problems with gluten is that it consists of proteins that are difficult to break down by our digestive enzymes. Gut bacteria are armed with a variety of enzymes and can completely or incompletely digest gluten. Complete degradation of gluten would be beneficial, but incomplete degradation by gut bacteria may increase the chances to develop celiac disease. In this proposal I will explore the role of gut bacteria isolated from patients with celiac disease and non celiac people in the digestion of dietary gluten and in the modulation of inflammation produced by this common protein in our diet. I propose that the bacteria that inhabit the gut of celiac patients have impaired capacity to digest gluten and that their enzymes produce toxic peptides from gluten that contribute to inflammation. Thus, celiac disease may be prevented, or better treated, by inhibiting these bacteria or their products.
Competitiondate
201503
Approvedterm2
5 yrs 0 mth
Pinamesdelim
Verdu, Elena F
Approvedterm
5 ans 0 mois
Cihrcontribution2
~ $648,752~ $0~