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Showing results for tags 'distinct'.
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Celiac Disease Shows Distinct Gut Biomarkers in Children
Scott Adams posted an article in Latest Research
Celiac.com 11/26/2020 - For all that recent research has told us about celiac disease, we still don't know whether changes in the intestinal microbiota of children with celiac disease contribute to the disease, or if they are a result of disease and/or its treatment with a gluten-free diet. A team of researchers recently conducted a study to better understand the issue. The research team included Konstantina Zafeiropoulou, Ben Nichols, Mary Mackinder, Olga Biskou, Eleni Rizou, Antonia Karanikolou, Clare Clark, Elaine Buchanan, Tracey Cardigan, Hazel Duncan, David Wands, Julie Russell, Richard Hansen, Richard K. Russell, Paraic McGrogan, Christine A. Edwards, Umer Z. Ijaz, and Konstantinos Gerasimidis. They are variously affiliated with the Human Nutrition, School of Medicine, Dentistry and Nursing, College of Medical, Veterinary and Life Sciences, University of Glasgow, New Lister Building, Glasgow Royal Infirmary, Glasgow, Scotland; the Department of Paediatric Gastroenterology, Royal Hospital for Children, Glasgow, Scotland, UK; and with the department of Civil Engineering, School of Engineering, University of Glasgow, Glasgow, Scotland, UK. The team assessed fecal samples from 57 healthy children, 20 children with new-onset celiac disease, 45 with celiac disease on a gluten-free diet, and 19 unaffected siblings of children with celiac disease in Glasgow, Scotland. The team used 16S ribosomal RNA sequencing to analyze samples, and gas chromatography to measure diet-related metabolites and looked at fecal samples from 13 children with new-onset celiac disease after 6 and 12 months on a gluten-free diet. They then assessed the connections between diet composition, microbiota, gastrointestinal function, and biomarkers of gluten-free diet compliance. Microbiota diversity was similar among the groups. The team saw no microbial dysbiosis in children with new-onset celiac disease. Most of the variation in microbiota composition was explained by the gluten-free diet. The difference in taxa between the groups was about a 3% to 5%, and celiac disease was marked by a specific microbe signature of eleven distinctive operational taxonomic units with high diagnostic probability. About 75% to 94% of the relevant differences between patients on a gluten-free diet with new-onset celiac disease vs healthy children were associated with nutrients and foods, and with biomarkers of gluten ingestion. Meanwhile, fecal levels of butyrate and ammonia decreased with a gluten-free diet. A number of the differences in the gut microbiota of children with established celiac disease appear to result from a gluten-free diet. Meanwhile, it's clear from the data that specific bacteria serve a distinct biomarkers of celiac disease. Further study will help to determine whether these bacteria contribute to celiac disease development. Read more in Gastroenterology- 1 comment
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Distinct Tooth Enamel Defects Can Help Reveal Celiac Disease
Jefferson Adams posted an article in Latest Research
Celiac.com 02/08/2017 - Celiac disease is a chronic autoimmune-mediated enteropathy, triggered by exposure to dietary gluten in genetically prone individuals. Celiac disease is also one of many gastrointestinal diseases that can have dental manifestations. In fact, distinct dental enamel defects are strong indicators of celiac disease, and may lead to a role for dentists in better celiac screening. While the disease often manifests in early childhood, a large number of patients are diagnosed over the age of 50. Despite increased awareness, the majority of patients still remain undiagnosed. Dentists should consider celiac disease when they observe certain symmetric enamel defects. Symptoms of celiac disease vary widely and are certainly not restricted to the intestine. They may include, among others, dental and oral manifestations. A team of researchers recently published an update in the British Dental Journal regarding the role of such defects in the timely diagnosis of celiac disease, which is requires a gluten-free diet to prevent complications. The research team included T. van Gils, H. S. Brand, N. K. H. de Boer, C. J. J. Mulder & G. Bouma. They are variously affiliated with the Department of Gastroenterology and Hepatology, VU University Medical Centre, Amsterdam, The Netherlands, and the Departments of Oral Biochemistry, Academic Centre for Dentistry Amsterdam (ACTA) in Amsterdam, The Netherlands. They note that most of the enamel defects are nonspecific, but symmetric in a way that is very specific to celiac disease. They also note the importance of recognizing this relationship, as it offers an easy way to help to identify unrecognized celiac sufferers, and to promote better screening and diagnosis. They encourage dental practitioners to take note. Source: British Dental Journal 222, 126 - 129 (2017). Published online: 27 January 2017 | doi:10.1038/sj.bdj.2017.80-
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Celiac.com 09/12/2016 - Wheat gluten and related proteins can trigger an autoimmune enteropathy, known as celiac disease, in people with genetic susceptibility. However, some people experience a range of gluten reaction symptoms, but without the classic blood or gut markers for celiac disease. The etiology and mechanism of these symptoms are unknown, and so far, researchers have found no biomarkers to explain the issue. A research team recently set out to determine if sensitivity to wheat in the absence of celiac disease is associated with systemic immune activation that may be linked to some type of enteropathy. The research team included Melanie Uhde, Mary Ajamian, Giacomo Caio, Roberto De Giorgio, Alyssa Indart, Peter H Green, Elizabeth C Verna, Umberto Volta, and Armin Alaedini. They are variously affiliated with the Celiac Disease Center and the Department of Medicine at Columbia University Medical Center, New York, New York, USA, Departments of Medical and Surgical Sciences and Digestive System, Centro di Ricerca Biomedica Applicata (C.R.B.A.), University of Bologna, St. Orsola-Malpighi Hospital, Bologna, Italy, and the Institute of Human Nutrition at Columbia University Medical Center, New York, New York, USA. The study included a group of healthy control subjects, patients with clinical celiac disease, and patients who reported symptoms after wheat consumption, but in whom doctors had ruled out celiac disease and wheat allergy. The team analyzed test samples for markers of intestinal cell damage and systemic immune response to microbial components. Patients with wheat sensitivity showed sharply increased serum levels of soluble CD14 and lipopolysaccharide (LPS)-binding protein, as well as antibody reactivity to bacterial LPS and flagellin. Circulating levels of fatty acid-binding protein 2 (FABP2), a marker of intestinal epithelial cell damage, were much higher in the affected individuals, and correlated with the immune responses to microbial products. Patients with wheat sensitivity who observed a gluten-free diet saw levels of FABP2 and immune activation markers move rapidly toward normal. These findings show a state of systemic immune activation, coupled with a compromised intestinal epithelium, that triggers gastrointestinal symptoms in certain individuals who have wheat sensitivity, but don't have celiac disease. Source: Gut. doi:10.1136/gutjnl-2016-311964
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Celiac.com 08/01/2016 - Symptoms and damage in celiac disease is caused by partially-degraded gluten peptides from wheat, barley and rye. Susceptibility genes are necessary to trigger celiac disease, but they can't do it alone. Some researchers suspect that these susceptibility genes might get help from conditions resulting from unfavorable changes in the microbiota. To better understand the whole picture, a team of researchers recently set out to examine gluten metabolism by opportunistic pathogens and commensal duodenal bacteria, and to characterize the ability of the resulting peptides to activate gluten-specific T-cells from celiac patients. The research team included A Caminero, HJ Galipeau, JL McCarville, CW Johnston, S Bernier, AK Russell, J Jury, AR Herran, J Casqueiro, JA Tye-Din, MG Surette, NA Magarvey, D Schuppan, and EF Verdu. They are variously affiliated with the Farncombe Family Digestive Health Research Institute, and the Department of Biochemistry & Biomedical Sciences, M. G. DeGroote Institute for Infectious Disease Research at McMaster University, Hamilton, Ontario, Canada; the Immunology Division, The Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade, Parkville, Victoria, Australia; the Department of Medical Biology, The University of Melbourne, Parkville, Victoria, Australia; Área de Microbiología, Facultad de Biología y Ciencias Ambientales, Universidad de León, León, 24071 Spain; the Immunology Division, The Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade, Parkville, Victoria, 3052 Australia; the Department of Gastroenterology, The Royal Melbourne Hospital, Grattan St., Parkville, Victoria, 3050 Australia, and the Institute for Translational Immunology and Research Center for Immunotherapy, University Medical Center, Johannes Gutenberg University, Mainz, Germany. For their study, the team colonized germ-free C57BL/6 mice with bacteria isolated from the small intestine of celiac patients or healthy controls, selected by their in vitro gluten-degrading capacity. They then measured gliadin levels and proteolytic action in intestinal contents after gluten feeding. Using peripheral blood mononuclear cells from celiac patients after receiving a 3-day gluten challenge, the research team characterized by LC-MS/MS the eptides produced by bacteria used in mouse colonizations from the immunogenic 33-mer gluten peptide. They found that the bacterial colonizations created clear gluten degradation patterns in the small intestine of the mice. Pseudomonas aeruginosa (Psa), an opportunistic pathogen from celiac patients, exhibited elastase activity and produced peptides that better translocated the mouse intestinal barrier. Psa-modified gluten peptides activated gluten-specific T-cells from celiac patients. In contrast, Lactobacillus spp. from the duodenum of non-celiac controls degraded gluten peptides produced by human and Psa proteases, reducing their immunogenicity. From these data, the research team concludes that small intestinal bacteria show clear gluten metabolic patterns in vivo, increasing or reducing gluten peptide immunogenicity. This microbe-gluten-host interaction may modulate autoimmune risk in genetically susceptible persons and may underlie any connection between celiac disease and microbial imbalance or maladaptation in the digestive tract. Source: Gastroenterology. 2016 Jun 30. pii: S0016-5085(16)34713-8. doi: 10.1053/j.gastro.2016.06.041.
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