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News Article | August 24, 2016
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About 40 percent of the population have a genetic disposition to celiac disease, but only about one percent develop the autoimmune condition when exposed to gluten, and this could be promoted by the type of bacteria present in the gut. Researchers at McMaster University have found that gluten, a common protein in the Western diet that is not well digested by the gut enzymes, could be metabolized by bacteria. The scientists of the Farncombe Family Digestive Health Research Institute at McMaster University discovered that mice that harbored in their gut the opportunistic bacteria Pseudomonas aeruginosa (Psa) isolated from celiac patients, metabolized gluten differently than mice treated with Lactobacillus, often used as probiotics. More interestingly, when the chemistry of gluten metabolism by Psa and Lactobacillus were analyzed, the researchers found that Psa produced gluten sequences that stimulated inflammation in celiac patients, while Lactobacillus was able to detoxify gluten. The paper, published online in the international medical journal Gastroenterology, was funded by a grant from the Canadian Institutes for Health Research and involved researchers in Canada, Australia and Germany. "So the type of bacteria that we have in our gut contributes to the digestion of gluten, and the way this digestion is performed could increase or decrease the chances of developing celiac disease in a person with genetic risk," said Elena Verdu, senior author of the study and an associate professor of medicine for the Michael G. DeGroote School of Medicine at McMaster. "Celiac disease is caused by gluten in genetically predisposed people, but bacteria in our gut could tip the balance in some people between developing the disease or staying healthy." Celiac disease is the inflammatory reaction triggered by eating gluten, which is a group of proteins found in wheat, rye and barley, and which leads to destruction of the gut lining. The number of people who suffer from celiac disease has been steadily increasing in the past decade, and some researchers feel it may be blamed on environmental factors. "We may be closer to understanding the way gut bacteria and opportunistic pathogens such as Psa could affect celiac disease risk. This will help us develop strategies to prevent these disorders, but more research is needed," said Verdu.

McClemens J.,Farncombe Family Digestive Health Research Institute
Clinical and vaccine immunology : CVI | Year: 2013

Enteric parasite infections around the world are a huge economic burden and decrease the quality of life for many people. The use of beneficial bacteria has attracted attention for their potential therapeutic applications in various diseases. However, the effects of beneficial bacteria in enteric parasitic infections remain largely unexplored. We investigated the effects of ingestion of Lactobacillus rhamnosus (JB-1) in a model of enteric nematode (Trichuris muris) infection. C57BL/6 (resistant to infection), AKR (susceptible to infection), interleukin 10 (IL-10) knockout (KO), and mucin Muc2 KO mice were infected with T. muris and treated orally with probiotic JB-1 or medium. The mice were sacrificed on various days postinfection to examine goblet cells, epithelial cell proliferation, cytokines, and worm burdens. Treatment with JB-1 significantly enhanced worm expulsion in resistant C57BL/6 mice, and this was associated with increases in IL-10 levels, goblet cell numbers, and epithelial cell proliferation. Beneficial effects of JB-1 were absent in IL-10 KO and resistant mice treated with γ-irradiated bacteria. Live JB-1 treatment also expedited worm expulsion in Muc2 KO mice and, more importantly, in AKR mice (susceptible to infection). Injection of IL-10 directly into the colonic tissue of uninfected mice induced goblet cell hyperplasia. These findings demonstrate that JB-1 modulates goblet cell biology and promotes parasite expulsion via an IL-10-mediated pathway and provide novel insights into probiotic effects on innate defense in nematode infection. Source

Oberc A.,McMaster University | Oberc A.,Michael G Degroote Institute For Infectious Disease Research | Coombes B.K.,McMaster University | Coombes B.K.,Michael G Degroote Institute For Infectious Disease Research | Coombes B.K.,Farncombe Family Digestive Health Research Institute
Frontiers in Immunology | Year: 2015

Crohn's disease (CD) is an immune-mediated intestinal illness that significantly compromises health in many developed countries. Although definitive causes remain elusive, the required contribution of microbes in the progression of disease has become an accepted concept. Known CD risk factors, such as antibiotic use and acute infectious gastroenteritis, may impact the gut. This concept is now being explored with a view toward understanding the beneficial and unfavorable microbes that may be altered in numbers during such external insults. A comprehensive understanding of the microbial component to CD could be useful clinically as future therapies may focus on preventing risk exposures on susceptible individuals, eliminating harmful microbes, or restoring a protective gut microbiome. Here, we examine how acute infectious gastroenteritis and antibiotic exposure may impact the gut microbiota in the context of inflammation in CD. © 2015 Oberc and Coombes. Source

Hall G.B.C.,McMaster University | Hall G.B.C.,Brain Body Institute | Kamath M.V.,McMaster University | Collins S.,McMaster University | And 7 more authors.
Neurogastroenterology and Motility | Year: 2010

Background Typically, conventional functional imaging methods involve repeated exposures to sensory stimulation. In rectal distension (RD) studies that involve multiple distensions, however, it is difficult to disambiguate the central response to RD from pathological alterations in peripheral neural responses associated with relaxation and accommodation of the rectum. Methods This study addressed potential confounders found in previous imaging studies by collecting functional magnetic resonance imaging studies (fMRI) data during a single slow ramp-tonic distension paradigm and analysing fMRI signal changes using independent component analysis. Key Results Compared with controls, IBS participants showed increased activation of the anterior cingulate cortices, insula and ventral medial prefrontal regions suggesting heightened affective responses to painful visceral stimuli. In addition, the failure by IBS patients to down-regulate activity within ventral medial prefrontal and the posterior cingulate/precuneus regions was suggestive of reduced sensitivity to somatic changes and delayed shifts away from rest in 'default network' activity patterns. Controls showed heightened activation of the thalamus, striatal regions and dorsolateral prefrontal cortex suggesting greater arousal and salience-driven sustained attention reactions and greater modulation of affective responses to discomfort and pain. Conclusion&Inferences This work points to alterations in the central response to visceral pain and discomfort in IBS, highlighting diminished modulation and heightened internalization of affective reactions. © 2009 Blackwell Publishing Ltd. Source

McPhee J.B.,McMaster University | Small C.L.,McMaster University | Reid-Yu S.A.,McMaster University | Brannon J.R.,McGill University | And 3 more authors.
Infection and Immunity | Year: 2014

Host defense peptides secreted by colonocytes and Paneth cells play a key role in innate host defenses in the gut. In Crohn's disease, the burden of tissue-associated Escherichia coli commonly increases at epithelial surfaces where host defense peptides concentrate, suggesting that this bacterial population might actively resist this mechanism of bacterial killing. Adherent-invasive E. coli (AIEC) is associated with Crohn's disease; however, the colonization determinants of AIEC in the inflamed gut are undefined. Here, we establish that host defense peptide resistance contributes to host colonization by Crohn's-associated AIEC. We identified a plasmid-encoded genomic island (called PI-6) in AIEC strain NRG857c that confers high-level resistance to α-helical cationic peptides and α-and β-defensins. Deletion of PI-6 sensitized strain NRG857c to these host defense molecules, reduced its competitive fitness in a mouse model of infection, and attenuated its ability to induce cecal pathology. This phenotype is due to two genes in PI-6, arlA, which encodes a Mig-14 family protein implicated in defensin resistance, and arlC, an OmpT family outer membrane protease. Implicit in these findings are new bacterial targets whose inhibition might limit AIEC burden and disease in the gut. © 2014, American Society for Microbiology. Source

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