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Found 3 results

  1. Celiac.com 04/17/2017 - A team of researchers recently set out to test this hypothesis and to gain insights into mechanisms underlying virus-induced loss of tolerance to dietary antigens. To do so, they developed a viral infection model that makes use of two reovirus strains that infect the intestine, but which differ in their immunopathological outcomes. The research team included Romain Bouziat, Reinhard Hinterleitner, Judy J. Brown, Jennifer E. Stencel-Baerenwald, Mine Ikizler, Toufic Mayassi, Marlies Meisel, Sangman M. Kim, Valentina Discepolo, Andrea J. Pruijssers, Jordan D. Ernest, Jason A. Iskarpatyoti, Léa M. M. Costes, Ian Lawrence, Brad A. Palanski, Mukund Varma, Matthew A. Zurenski, Solomiia Khomandiak, Nicole McAllister, Pavithra Aravamudhan, Karl W. Boehme, Fengling Hu, Janneke N. Samsom, Hans-Christian Reinecker, Sonia S. Kupfer, Stefano Guandalini, Carol E. Semrad, Valérie Abadie, Chaitan Khosla, Luis B. Barreiro, Ramnik J. Xavier, Aylwin Ng, Terence S. Dermody, and Bana Jabri. Reoviruses usually infect humans and mice without overt physical symptoms. Prior research by Bouziat et al., has shown that immune responses to two gut-infecting reoviruses take different paths in mice, as noted in the Perspective by Verdu and Caminero. Both reoviruses triggered protective immune responses. However, when one of the reoviruses occurred in the presence of a dietary antigen, such as gluten or ovalbumin, tolerance to the dietary antigen disappeared. This was because this strain blocked the formation of tolerogenic T cells. Instead, it promoted T helper 1 immunity to the dietary antigen through interferon regulatory factor 1 signaling. Moreover, celiac disease patients also showed elevated levels of antibodies against reovirus. Reovirus is an avirulent pathogen that elicits protective immunity, but these researcher have shown that it can also cause a disruption of intestinal immune homeostasis at inductive and effector sites of oral tolerance by suppressing peripheral regulatory T cell (pTreg) conversion, and promoting TH1 immunity to dietary antigen. TH1 immunity to dietary antigen depended on interferon regulatory factor 1, and was unconnected to suppression of pTreg conversion, which was mediated by type-1 interferon. This study provides important scientific support for the idea that this seemingly mild reovirus plays a major role in the development of celiac disease. Clearly further study is needed to determine the exact nature of the role of reovirus in celiac disease, and to determine if these connections might prompt any changes in celiac diagnosis and treatment. Source: Science 07 Apr 2017: Vol. 36, Issue 6333, pp. 44-50. DOI: 10.1126/science.aah5298 The researchers are variously affiliated with the Department of Medicine, the Department of Pathology, and the Committee on Immunology at the University of Chicago in Chicago, IL, USA; the Department of Pathology, Microbiology, and Immunology, the Department of Pediatrics, and the Elizabeth B. Lamb Center for Pediatric Research at Vanderbilt University Medical Center in Nashville, TN, USA; the Department of Translational Medical Sciences, Section of Pediatrics, University of Naples Federico II, and CeInGe–Biotecnologie Avanzate, Naples, Italy; the Laboratory of Pediatrics, Division of Gastroenterology and Nutrition, Erasmus University Medical Center Rotterdam-Sophia Children’s Hospital, Rotterdam, Netherlands; the Department of Chemistry, Stanford University, Stanford, CA, USA; the Division of Gastroenterology, Department of Medicine, Gastrointestinal Unit and Center for the Study of Inflammatory Bowel Disease, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; the Broad Institute of MIT and Harvard University, Cambridge, MA, USA; the University of Chicago Celiac Disease Center at the University of Chicago, Chicago, IL, USA; the Section of Gastroenterology, Hepatology, and Nutrition, Department of Pediatrics, University of Chicago, Chicago, IL, USA; the Department of Microbiology, Infectiology, and Immunology, University of Montreal, and the Centre Hospitalier Universitaire (CHU) Sainte-Justine Research Center, Montreal, Quebec, Canada; the Department of Chemical Engineering, Stanford University, Stanford, CA, USA; the Stanford ChEM-H, Stanford University, Stanford, California, USA; the Department of Genetics, CHU Sainte-Justine Research Center, Montreal, Quebec, Canada; the Center for Computational and Integrative Biology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; the Department of Pediatrics, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA; and the Department of Microbiology and Molecular Genetics, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
  2. Hi All- I am currently recovering from my first stomach flu post diagnosis and eliminating gluten (~7 mo post dx); having all this free time has me wondering: Have you noticed a difference in your stomach flu recovery times pre and post gluten-free? Anecdotally, I seem to be having a harder time recovering from this virus than anything I experienced when I was eating gluten. It could very well just be the viciousness of this particular bug, but I am 10 days out from the onset of symptoms and am still feeling crummy (occasional nauseousness, little to no appetite flare in constipation). Does anyone else have an experience they would like to share? Do celiacs have longer recovery times as a rule of thumb? Thanks and best to you all -Laurie
  3. Celiac.com 03/22/2010 - The main cause for gluten intolerance continues to puzzle scientists, but pathogenesis theories include both genetic susceptibility and environmental triggers, like a virus or infection. For the first time, scientists working with the Academy of Finland’s Research Program on Nutrition, Food, and Health have found genes in the body that are associated both with the immune system and with the body's ability to properly digest gluten in the intestinal tract. Gluten intolerance arises from an autoimmune reaction in the small intestine to the gluten protein found in wheat, barley and rye. Academy Research Fellow Paivi Saavalainen, a veteran researcher in hereditary risk factors for gluten intolerance, says that "some of the genes we have identified are linked with human immune defense against viruses. This may indicate that virus infections may be connected in some way with the onset of gluten intolerance.” Data shows that rates of celiac disease in America have increased more than 400% since World War II. Meanwhile, a Finnish scientist internationally known for his gluten research says that the number of people in Finland who suffer from gluten intolerance has doubled over the last two decades. Since the early 1980s, the percentage of Finns with gluten intolerance has risen from about 1 percent of adults to about 2 percent, according to Professor Markku Mäki, head of a research project in the Academy of Finland's Research Program on Nutrition, Food and Health. "We've already seen a similar trend emerge earlier on where allergies and certain autoimmune disorders are concerned. Screening has shown that gluten intolerance occurs in 1.5 per cent of Finnish children and 2.7 per cent of the elderly. The higher figure for older people is explained by the fact that the condition becomes more frequent with age," says Mäki. For the immune study, when researchers scanned the genetic maps of more than 9400 celiac patients, they found areas of immune system disturbance. Their evidence also indicated that genes connected with the inability to digest gluten were also connected with other autoimmune diseases such as type 1 diabetes and rheumatoid arthritis. Saavalainen and his team have succeeded in localizing risk genes in both individual patients and entire families, which adds weight to the notion that gluten intolerance is inherited. The researchers are hoping to use the genetic information to craft better screening tests for gluten intolerance, as up to 75% of people with gluten intolerance remain undiagnosed due to mild or atypical symptoms, and many with condition may unwittingly suffer damage to their intestinal villi. Professor Maki points out that many present first with iron deficient, or folic acid deficient, anemia. Source: Academy of Finland