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Found 16 results

  1. Celiac.com 02/29/2016 - Previous studies have shown that oat proteins trigger an adverse anti-33-mer monoclonal antibody reaction that is proportional to the immune responses in terms of T-cell proliferation. Although there has been some research regarding the impact of these varieties on the adaptive response, researchers still don't know very much about the role of the dendritic cells. A research team recently set out to characterize different oat fractions and to study their effect on dendritic cells from celiac patients. The research team included Isabel Comino, David Bernardo, Emmanuelle Bancel, María de Lourdes Moreno, Borja Sánchez, Francisco Barro, Tanja Šuligoj, Paul J. Ciclitira, Ángel Cebolla, Stella C. Knight, Gérard Branlard and Carolina Sousa. They are variously affiliated with the Departamento de Microbiología y Parasitología, Facultad de Farmacia, Universidad de Sevilla, Sevilla, Spain; the Gastroenterology Unit, Antigen Presentation Research Group, Imperial College London & St Mark′s Hospital, Harrow, United Kingdom; the Hospital Universitario de La Princesa and Instituto de Investigación Sanitaria Princesa (IIS-IP), Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBEREHD), Madrid, Spain; the INRA UMR-1095, Clermont-Ferrand, France; the Nutrition and Bromatology Group, Department of Analytical and Food Chemistry, Food Science and Technology Faculty, University of Vigo-Ourense Campus, Ourense, Spain; the Instituto de Agricultura Sostenible (CSIC), Córdoba, Spain; the Division of Diabetes and Nutritional Sciences, King's College London, Gastroenterology, The Rayne Institute, St Thomas' Hospital, London, United Kingdom; and the Biomedal S.L., Sevilla, Spain. The team first isolated protein fragments from oat grains and then analyzed them using SDS–PAGE. They then characterized several proteins in the prolamin fraction using immunological and proteomic tools, as well as Nano-LC-MS/MS. These proteins were very similar to α- and γ-gliadin, and showed reactive sequences to anti-33-mer antibody, indicating their potential for causing adverse immune reactions. Furthermore, the team found that some of the newly identified oat peptides triggered a range of immune responses on circulating dendritic cells from celiac patients, as compared with healthy controls. This is the first study to show that newly identified oat peptides can trigger a range of stimulatory responses on circulating dendritic cells from celiac patients, which highlights the potential of these oat peptides to trigger adverse immune responses in people with celiac disease. Source: Food & Nutrition Research eISSN 1654-661X
  2. Celiac.com 12/21/2012 - Over the past several years, researchers have made substantial progress in understanding the causes of autism, which now afflicts about 1 in 88 children. However, very little news of this progress seems to have spread into popular consciousness, much of which continues to focus on the possible role of vaccines. Recent discoveries indicates that one-third or more cases of autism look to be a kind of inflammatory disease, which begins well before birth. In the August 25th issue of the New York Times, Moises Velasquez-Manhoff has very interesting article in which he discusses the widening view among researchers that autism is, in fact, an inflammatory disease. The article is long and comprehensive, and cites numerous studies, findings and experiments. Inflammation is the body's natural response to certain kinds of threats. In a normal body, the immune system uses inflammation in a very precise, targeted way, before returning to a normal state. In autistic individuals, inflammatory signals become the dominant condition, and there is no balancing anti-inflammatory response. A state of chronic inflammation becomes normal. And the more skewed toward inflammation, the more acute the autistic symptoms. This inflammatory deregulation adversely impacts the brains of autistic individuals. Velasquez-Manhoff also cites a number of studies that trace these inflammatory effects back to the inflammatory responses of the mother during pregnancy. Among the studies cited in the article is a population-wide study from Denmark spanning two decades of births, which indicates that infection during pregnancy increases the risk of autism in the child. The study found that hospitalization for a viral infection, like the flu, during the first trimester of pregnancy triples the odds of autism. Bacterial infection, including of the urinary tract, during the second trimester increases chances by 40 percent. Another large Danish study, which included nearly 700,000 births over a decade, found that a mother’s rheumatoid arthritis, a degenerative disease of the joints, elevated a child’s risk of autism by 80 percent. Rates of autism in children of mothers with celiac disease were 350 percent higher than normal. Genetic studies had similar findings. Variations in genes associated with regulating the immune system also increase the risk of autism, especially when they occur in the mother. A mother’s diagnosis of asthma or allergies during the second trimester of pregnancy increases her child’s risk of autism. So does metabolic syndrome, a disorder associated with insulin resistance, obesity and, crucially, low-grade inflammation. Yet, viral and bacterials infections themselves do not seem the cause of the autism epidemic. The epidemiology doesn’t support that conclusion. A far more likely culprit is maternal immune dysregulation. Basically, the mother’s attempt to repel invaders, her inflammatory response, seems to be at fault. Research by Paul Patterson, an expert in neuroimmunity at Caltech, supports this idea. In his research, he introduces inflammation in pregnant mice artificially, without a live infection. This causes behavioral problems in the young. In this model, autism results from collateral damage. It’s an unintended consequence of self-defense during pregnancy. Since infantile autism was first described by Leo Kanner in 1943, diagnoses have risen tenfold. During that same period, viral and bacterial infections generally declined. However, overall rates of inflammatory diseases have risen sharply since then. As a group, these diseases include asthma, now estimated to affect 1 in 10 children, rates that have at least doubled since 1980, along with autoimmune disorders, which now afflict 1 in 20. Recently, William Parker at Duke University has chimed in. Some years back, he began comparing wild sewer rats with clean lab rats. The bodies of wild rats tightly controlled inflammation, but those of the lab rats did not. Parker found that the bodies of the wild rats contained high levels of parasites. Parasites are noted for limiting inflammation. One lesson from these rodent experiments is that fixing the maternal dysregulation will most likely prevent autism. That theory is supported by Swiss researchers, who created a lineage of mice with a genetically reinforced anti-inflammatory signal. They then inflamed the pregnant mice. The babies emerged fine, with no behavioral problems. This suggests that if inflammation is controlled during pregnancy, it won’t interfere with fetal brain development. Interestingly, asthma researchers are coming to similar conclusions: preventing inflammation in pregnant women will likely prevent asthma. Dr. Parker has introduced a more aggressive approach. He suggests that by using specially developed worms to restore “domesticated” parasites doctors can correct immune dysregulation. To determine if this is feasible, a trial is under way at the Montefiore Medical Center and the Albert Einstein College of Medicine. The trial is using a medicalized parasite called Trichuris suis, known as a whipworm, to treat autistic adults. The whipworm is native to pigs, and was first used medically to treat inflammatory bowel disease. It has shown anecdotal benefit in autistic children. The article suggests that the future of treating immune dysregulation, and thus preventing diseases like autism and asthma, may lie in reintroducing parasites into the human body. Stay tuned for more updates on this truly fascinating science. Read the full article by Moises Velasquez-Manhoff in the New York Times.
  3. This article appeared in the Winter 2007 edition of Celiac.coms Scott-Free Newsletter. Celiac.com 04/26/2007 - My fingernails were shredding and I was a bit out of it mentally, missing obvious things. I’ve had to stop eating many foods because I have intolerances to almost everything I used to eat before I went gluten-free, and I wondered if I had dropped some essential nutrients when I cleared all of those foods out of my diet. So I checked my diet for nutrient deficiencies, using the USDA nutrients database at www.nal.usda.gov/fnic/foodcomp/search. I’m sure there’s software that works with this database but I wrote a little computer program to analyze my diet. I have an electronic food scale, so weighing food is easy. The most important thing I found is that I’m low on vitamin D. You can get vitamin D from food, or from a supplement, and from the ultraviolet B in sunlight; many of us, like me, may get almost none from any of those sources. And—this is important for a lot of us—vitamin D deficiency can cause a lot of symptoms including immune system problems! I went looking on Medline and it was mentioned as having anti-inflammatory properties, as preventing cancers such as colon cancer and lymphoma; preventing infections, and helping with autoimmune diseases. Gluten intolerance is less common in the middle east and more common in northern Europe. I’ve seen this explained as the result of evolution, since wheat has been used for longer in the Middle East. But I wonder if people in the north are also more likely to be gluten intolerant (an autoimmune disease) because they don’t get as much vitamin D. It may also explain why people get more colds during the winter season when there’s less sunlight. Vitamin D deficiency is best known for causing rickets in children and osteomalacia (softened bones, muscle weakness and pain, tender sternum) in adults. Osteomalacia is often misdiagnosed as fibromyalgia, because the symptoms are similar. Rickets is increasing in the U.S., especially among black children. Most post-menopausal bone loss in women occurs during the winter. It can take months of increased vitamin D intake to correct the health problems caused by deficiency. There are only a few significant dietary sources of vitamin D. In the U.S., almost all milk is fortified with vitamin D to 100 IU per cup, so you should get the recommended daily intake of 400 IU if you drink 4 cups of milk per day. However, milk often doesn’t have as much vitamin D as is claimed on the label. Some cereals, like Kellogg’s Cornflakes, have small amounts of added vitamin D. Typically, 10 cups of fortified cereal would give you the RDI. The government encourages fortification of milk and cereal so that fewer children will develop rickets. Otherwise—you would get the RDI from nine oysters, or about 4 ounces of fatty fish like salmon or tuna, or a teaspoon of cod liver oil. Many other kinds of fish have only small amounts. You’d have to eat 2 pounds of cod to get the RDI. The only natural vegan source of vitamin D is Shiitake mushrooms. Just like people, mushrooms make vitamin D when they’re exposed to ultraviolet. About 13 sun-dried shiitake mushrooms contain the RDI. And that’s it. Many of us on gluten-free diets are also not eating dairy or fortified cereals, so unless we have a passionate love-affair with fish or oysters or shiitake, we would be getting almost no vitamin D from food. You can get vitamin D the natural way, from the sun. It takes exposure to sunlight outside (not under glass) on your hands and feet for about fifteen minutes a day. I was not sure what was meant by “direct sunlight”. I read someplace that ultraviolet is scattered over the whole sky. Unlike visible light, the whole sky shines with ultraviolet. Clouds would filter out some of it. People with dark skin require more time in the sun, so many black people develop a deficiency. Using even low-SPF sunscreen prevents your body from making vitamin D. The farther from the equator you live, the less UVB there is in the winter sunlight, because the sun is closer to the horizon in the winter and the sunlight filters through more atmosphere before it gets to you. At the latitude of Boston, and near sea level, there isn’t enough UVB radiation between November and February for one’s body to make vitamin D. You have probably heard the public health advice to wear sunscreen—the same ultraviolet B that generates vitamin D in your body also causes skin cancer and ages skin. The small amount of exposure to sunlight required is probably only a very small cancer risk and would cause little photo-aging of the skin. Unfortunately I wasn’t able to find quantitative information about how carcinogenic fifteen minutes’ daily sun exposure would be. There are also vitamin D lights, which are probably also a healthful choice. I have severe immune system problems. I tested positive for 53 inhalant allergies—my body had developed allergies to almost all the allergens around. I get sick for days if I eat almost any of the foods that I ate while I was eating gluten. I even get sick from a couple of foods that, so far as I can remember, I only started eating on a gluten-free diet. So I live on an exotic-foods diet. I’ve had a hellish time trying to get allergy shots. At a concentration of 1 part in 10 million they make me sick for a couple of days while the normal starting concentration for allergy shots is 1 in 100,000. I’m plagued by bladder infections. With cranberries being one of my intolerances, I can’t even use them to help prevent the infections. I’ve certainly been short of vitamin D. I live in the north, and I’m always careful to use high-SPF sunscreen when I go outdoors. I can’t eat milk, fish, shellfish or mushrooms, so I can’t get a significant amount of vitamin D from food. I haven’t been taking any vitamin supplements, because almost all have traces of protein from some food that makes me sick. It would be lovely if vitamin D deficiency turned out to be part of the cause of my very burdensome immune problems. I’m skeptical because I was getting vitamin D from a supplement and/or from my diet up until 2 years ago, when I found I had a vast number of hidden food intolerances, and I started having reactions to vitamin pills. Fortunately there is a vitamin D supplement that I can take—vitamin D3 made by Pure Encapsulations. The ingredients in the capsule are made from wool and pine trees. I’ll find out if it helps over the next few months. Vitamin D causes disease when taken in large amounts, so if you think you are deficient, don’t take too much to make up for it. Vitamin D is a hormone—it’s not something to take in mega-doses, any more than, hopefully, one would take a mega-dose of estrogen or testosterone. If your doctor recommends a high dose, they should do regular blood tests to keep track of your vitamin D level. It’s pretty safe to take up to 2000 IU per day on your own. Dr. Michael Holick, a vitamin D researcher at Boston University and author of The UV Advantage, believes that people need about 1000 IU per day. I asked a family doctor, who said they suggest 400-800 IU per day for middle-aged women. However, it might be a good idea for gluten intolerant people to take more, about 1000 - 2000 IU per day, since we may have difficulties absorbing vitamins and celiac disease is an autoimmune disease. Vitamin D is very important, just as all the vitamins are. But we are conditioned by the media, and tend to think more about vitamins C and E, which get a lot of attention because they’re antioxidants. Vitamin D was the absolutely last one I looked at. Then I found that it was my most serious deficiency! And nutrient deficiencies are not a trendy topic, so the possibility of developing deficiencies is something people tend to forget while trying to improve their diets. Many people who avoid gluten also have other food intolerances, or are on some other kind of special diet, and it would be an excellent idea to go to the USDA database and find out whether their new diet is giving them enough vitamins and minerals. It certainly helped me. I feel more cheerful and alert, like my mind woke up on a sunny day. It’s best to get as much as possible from one’s diet, too. Whole foods have a lot in them that’s good for the body that research hasn’t yet identified, and if your diet gives you the RDA of all the vitamins and minerals, it will also be giving you other healthful nutrients that will do you a lot of good. This might also be true of vitamin D. Maybe it’s better to get a small amount of ultraviolet, like an iguana sitting under a UV lamp, instead of taking pills. UVB might be healthy in ways we don’t yet know about. Vitamin D is a bit like stored-up sunlight. You can catch it for yourself from the sun when it’s high in the sky, you can eat the sunlight the fish have gathered for you, or you can take a supplement and keep packed sunlight on your shelf.
  4. Celiac.com 11/12/2012 - For the first time, researchers looking for a link between gluten and the immune system have been able to visualize the connection, according to new research in the scientific journal, Immunity. The discovery may help to pave the way for a treatment for celiac disease that can restore immune tolerance to gluten and allow patients to return to a normal diet including gluten. Such a treatment would certainly be welcome news to many people who suffer from celiac disease. The breakthrough is the result of a collective effort by researchers in Australia, the Netherlands and at Cambridge, Massachusetts-based ImmusanT Inc. The project was led by Professor Jamie Rossjohn and Dr. Hugh Reid at Monash University, Dr. Bob Anderson of ImmusanT and Professor Frits Koning at the University of Leiden. By using x-ray crystallography, the researchers were able visualize the way in which T cells interact with the gluten protein that cause celiac disease in patients with the DQ8 susceptibility gene. This discovery will help researchers better understand how celiac disease is triggered, and how pathology develops at the cellular level. About half the population carries the immune response genes HLA-DQ2 or HLA-DQ8, making them genetically susceptible to celiac disease. At least one in 20 people who have the HLA-DQ2 gene, and about one in 150 who carry HLA-DQ8 will develop celiac disease, but people with other versions of the HLA-DQ genes seem to be protected from it. This fact made researchers wonder how the immune system can sense gluten. That wondering triggered research efforts that led to an answer. An important one. “This is the first time that the intricacies of the interaction between gluten and two proteins that initiate immune responses have been visualized at a sub-molecular level. It is an important breakthrough for celiac disease and autoimmune disease,” stated Professor Jamie Rossjohn, National Health and Medical Research Fellow, Monash University. The researchers used the Australian three GeV Synchrotron to determine how T-cells of the immune system interact with gluten. Unlike an accelerator such as the LHC, the Australian Synchroton is a light source rather than a collider, making it ideal for the new study. The end goal of the project is to produce a treatment which allows celiac sufferers to resume a normal diet. Understanding the gluten peptides responsible for celiac disease offers what Dr. Bob Anderson, ImmusanT's Chief Scientific Officer, calls "unique opportunity to interrogate the molecular events leading to a[n]...immune response.” To address this opportunity, ImmusanT is currently developing a blood test and a therapeutic vaccine, Nexvax2, for celiac disease patients who carry HLA-DQ2. Nexvax2 uses three gluten peptides commonly recognized by gluten-reactive T cells. Nexvax2 is intended to restore immune tolerance to gluten and allow patients to return to a normal diet including gluten. Future studies will investigate whether T cell activation by gluten in patients with HLA-DQ2 follows similar principles. If it were safe and effective, would you consider a treatment that restored your immune tolerance to gluten and allowed you to eat a normal diet including gluten? Comment below to let us know your thoughts. Source: Immunity
  5. Celiac.com 06/07/2013 - A number of studies have indicated that people with celiac disease have an inadequate response to hepatitis B vaccination. In an effort to better understand the issue, a team of researchers recently set out to assess hepatitis B vaccination response in relation to gluten exposure status in patients with celiac disease. The research team included F. Zingone, P. Capone, R. Tortora, A. Rispo, F. Morisco, N. Caporaso, N. Imperatore, G. De Stefano, P. Iovino, and C. Ciacci. They are affiliated with the Department of Medicine and Surgery at the University of Salerno in Salerno, Italy. To measure the gluten exposure status at the time of vaccination, they compare three groups of patients, along with a control group. In all, the study included 163 celiac patients. Group A contained 57 patients exposed to gluten, including patients vaccinated as 12-year-old adolescents, for whom celiac disease diagnosis was established after vaccination. Group B contained 46 patients not exposed to gluten, including patients vaccinated as 12-year-old adolescents and on a gluten-free diet at the time of vaccination. Group C was composed of 60 infants, including those vaccinated at birth. Group D included 48 healthy, vaccinated, non-celiac subjects. The researchers then compared the response of celiac patients to hepatitis B vaccination with the response by healthy subjects. They found that 43.9% of patients in group A, 34.8% of patients in group B, 58.3% of patients in group C, and 8.3% of patients in group D showed inadequate response to hepatitis B immunization. Overall, group A versus group D, P less than 0.001; group B versus group D, P = 0.002; group C versus group D, P = 0.001, while they found no significant difference for group A versus group B and group A versus group C. This study suggests that gluten exposure does not influence the response to hepatitis B immunization, and that the human leukocyte antigen likely plays the main immunological role in poor responses to hepatitis B-vaccinated celiac patients. Source: Clin Vaccine Immunol. 2013 May;20(5):660-2. doi: 10.1128/CVI.00729-12. Epub 2013 Feb 27.
  6. Celiac.com 12/31/2012 - In people with celiac disease, eating wheat, barley, or rye triggers inflammation in the small intestine. Left unchecked, this inflammation causes the gut damage that is associated with untreated celiac disease. Specifically, the storage proteins in these grains (gluten) trigger an adaptive Th1-mediated immune response in individuals carrying HLA-DQ2 or HLA-DQ8 as major genetic predisposition. Researchers actually have a pretty good understanding of this aspect of celiac disease, part of a process called adaptive immunity. However, there has been some research that suggests that gluten proteins might trigger an immune response in people who do not have celiac disease, and who do not carry the HLA-DQ2 or HLA-DQ8 genetic markers that predispose them to developing celiac disease. Such a response is part of a process called innate immunity, and is far less understood than the adaptive immunity process. The innate immune system provides an early response to many microbial and chemical stimuli and is critical for successful priming of adaptive immunity. To better understand the relationship between adaptive immunity and innate immunity in celiac disease, a research team recently set out to determine if gliadin digests might induce innate immune responses in celiac and non-celiac individuals. Specifically, they wanted to know if wheat amylase trypsin inhibitors drive intestinal inflammation, and if so, by what receptor mechanism. The research team included Yvonne Junker, Sebastian Zeissig, Seong-Jun Kim, Donatella Barisani, Herbert Wieser, Daniel A. Leffler, Victor Zevallos, Towia A. Libermann, Simon Dillon, Tobias L. Freitag, Ciaran P. Kelly, and Detlef Schuppan. They are affiliated variously with the Division of Gastroenterology and the Proteomics and Genomics Center at Beth Israel Deaconess Medical Center at Harvard Medical School in Boston, with the Department of General Pediatrics and the Department of Internal Medicine I at the University Medical Center Schleswig-Holstein Kiel in Kiel, Germany, the Department of Experimental Medicine at the University of Milano-Bicocca in Milan, Italy, the German Research Center for Food Chemistry in Garching, Germany, the Hans-Dieter-Belitz-Institute for Cereal Grain Research in Freising, Germany, the Division of Molecular and Translational Medicine in the Department of Medicine I at Johannes Gutenberg University in Mainz, Germany, and with the Department of Bacteriology and Immunology at the Haartman Institute at the University of Helsinki in Finland. A number of earlier studies (Molberg et al., 1998; Anderson et al., 2000; Shan et al., 2002) have found HLA-DQ2– and HLA-DQ8–restricted gluten peptides that trigger the adaptive immune response in people with celiac disease. However, only 2–5% of individuals who show these HLAs develop celiac disease, which means that other factors, especially innate immune activation, are at play in the generation of celiac disease. Responsive innate cells are primarily macrophages, monocytes, DCs, and polymorphonuclear leukocytes that by means of their pattern-recognition receptors, such as TLRs, trigger the release of proinflammatory cytokines and chemokines, resulting in recruitment and activation of additional inflammatory cells (Medzhitov, 2007). Earlier studies (Maiuri et al., 2003) showed that peptides p31-43 or p31-49 from α-gliadin, that lack adaptive stimulatory capacity, triggered innate immune reactions by inducing IL-15 and Cox-2 expression in patient biopsies, and MHC class I polypeptide–related sequence A (MICA) on intestinal epithelial cells (Hüe et al., 2004). However, these studies have proven difficult to reproduce in cell culture, and researchers could not identify any specific receptor responsible for the observed effects. In a subsequent study, gliadin, in cell culture, reportedly triggered increased expression of co-stimulatory molecules and the production of proinflammatory cytokines in monocytes and DCs (Nikulina et al., 2004; Cinova et al., 2007). Two other studies (Thomas et al., 2006; Lammers et al., 2008) implicated the chemokine receptor CXCR3 in increased intestinal epithelial permeability upon gliadin challenge in a MyD88-dependent manner. However, those studies failed to reproducibly identify a specific gliadin peptide as the trigger. So far, no clear picture of the role of the innate immune system in celiac disease has emerged. In this study, the researchers show that members of the non-gluten α-amylase/trypsin inhibitors (ATIs), CM3 and 0.19, pest resistance molecules in wheat and related cereals, are strong triggers of innate immune responses in human and murine macrophages, monocytes, and dendritic cells. Their results show that ATIs activate the TLR4–MD2–CD14 complex and lead to up-regulation of maturation markers and elicit release of proinflammatory cytokines in cells from celiac and nonceliac patients and in celiac patients’ biopsies. They also show that mice deficient in TLR4 or TLR4 signaling are protected from intestinal and systemic immune responses upon oral challenge with ATIs. These findings define cereal ATIs as novel contributors to celiac disease. Moreover, ATIs may fuel inflammation and immune reactions in other intestinal and nonintestinal immune disorders. The findings of this study mean that the proteins in wheat may trigger immune reactions not just in people with celiac disease, but in people without celiac disease, and that these reactions may be actively contributing to the development of numerous other intestinal and non-intestinal immune disorders. That's a pretty big deal. Stay tuned to see how future studies elaborate these findings. Read the entire study in the Journal of Experimental Medicine. Source: J Exp Med. 2012 Dec 17;209(13):2395-408. doi: 10.1084/jem.20102660
  7. Celiac.com 08/13/2012 - Research has indicated that giving small amounts of wheat-rich food to people with celiac disease, who are on a gluten-free diet, will trigger interferon (IFN)-γ-secreting T cells in the bloodstream. These T cells react to gluten, and can be easily detected. However, very little is known about how this procedure might be reproduced in the same patient groups that underwent two, or more, gluten challenges. A team of researchers recently set out to assess the reproducability of this short wheat challenge method for detecting immune an response to gluten. The research team included A. Camarca, G. Radano, R. Di Mase, G. Terrone, F. Maurano, S. Auricchio, R. Troncone, L. Greco, C. Gianfrani. They are affiliated with the Institute of Food Sciences-CNR, Avellino Department of Paediatrics and European Laboratory for the Investigation of Food-Induced Diseases, University of Naples, Naples, Italy. They evaluated fourteen celiac patients in remission who consumed wheat bread for 3 days, along with thirteen patients who underwent a second gluten challenge after 3-10 months on a strict gluten-free diet. The team then analyzed the immune reactivity to gluten in peripheral blood by detecting IFN-γ both before and 6 days after patients began a a gluten-inclusive diet. They found that gliadin-specific IFN-γ-secreting CD4(+) T cells increased significantly by day 6 of the first challenge. These cells arose as prevalently human leucocyte antigen (HLA)-DQ restricted and with a phenotype of gut homing, as suggested by the expression of β7-integrin. They also saw a reaction to gliadin after the second wheat consumption, although the responses varied by individual at each challenge. The study showed that a short wheat challenge offers a non-invasive approach to investigate the gluten-related immune response in peripheral blood of people who are sensitive to gluten. Moreover, the study showed that the procedure can be reproduced in the same subjects after a gluten wash-out of at least 3 months. The results of this study mean that we can likely expect this procedure to find its way into clinical practice in the future. Source: Clinical and Experimental Immunology. 2012 Aug;169(2):129-36. doi: 10.1111/j.1365-2249.2012.04597.x.
  8. Celiac.com 03/28/2012 - A clinical research team wanted to determine if adding ascorbate (vitamin C) to gliadin-stimulated biopsy culture could reduce the mucosal immune response to gliadin in people with celiac disease. The research team included D. Bernardo, B. Martínez-Abad, S. Vallejo-Diez, E. Montalvillo, V. Benito, B. Anta, L. Fernández-Salazar, A. Blanco-Quirós, J. A. Garrote, and E. Arranz. They are affiliated with the Mucosal Immunology Lab of the Department of Paediatrics & Immunology at Spain's Universidad de Valladolid-CSIC. Their quest was fueled by the understanding that the IL-15/NF-κB axis plays a key role in celiac disease. Because ascorbate is known to inhibit effects on NF-κB, the IL-15/NFκB axis looks like a good possible molecular target for reducing gliadin-induced inflammation in celiac disease. For their study, the team conducted in vitro gliadin challenges (100 μg/ml) on duodenal biopsy explants from treated patients with celiac disease. Challenges were conducted with and without 20mM ascorbate. As an internal control, the team used an extra tissue explant in basal culture. The team then measured secretion levels of nitrites (3h), and IFNγ, TNFα, IFNα, IL-17, IL-13, and IL-6 (24h) on the supernatants. They measured IL-15 using western-blot on whole protein duodenal explants. When the team added ascorbate to in vitro culture gliadin-challenged biopsies, they found that the ascorbate blocked secretion of nitrites (p=0.013), IFNγ (p=0.0207), TNFα (p=0.0099), IFNα (p=0.0375), and IL-6 (p=0.0036), as compared with samples from culture that received no ascorbate. They also found that the addition of ascorbate reduced cytokine secretion to levels even lower than those observed in basal cultures (IFNγ: p=0.0312; TNFα: p=0.0312; IFNα: p=0.0312; and IL-6: p=0.0078). Moreover, the gliadin-challenge triggered IL-15 production in biopsies from treated celiac disease patients, while IL-15 was completely blocked in the cultures that received ascorbate. Interestingly, ascorbate completely blocked IL-15 production even in the only treated celiac disease-patient who showed basal IL-15 production. From these results, the team concludes that ascorbate reduces the mucosal inflammatory response to gluten in an in vitro biopsy culture. As such, ascorbate might offer supplementary benefits in future celiac disease therapy. Source: Allergol Immunopathol (Madr). 2012 Jan-Feb;40(1):3-8.
  9. Celiac.com 09/13/2010 - What's happening in with the immune system when a child is first diagnosed with celiac disease? What happens when they are treated with a gluten-free diet? Some recent studies have indicated that both the adaptive and the innate immune system play roles in celiac disease. However, until now, doctors haven't known much about the immune phenotype of children with celiac disease and how that phenotype might by affected by a gluten-free diet. To move toward a better understanding of these issues, a team of researchers recently studied immune phenotype in children with either newly diagnosed celiac disease, or celiac disease treated with a gluten-free diet. The research team included Áron Cseh, Barna Vásárhelyi, Balázs Szalay, Kriszta Molnár, Dorottya Nagy-Szakál, András Treszl, Ádám Vannay, András Arató, Tivadar Tulassay and Gábor Veres. The are affiliated with the First Department of Pediatrics in the Research Group for Pediatrics and Nephrology at Semmelweis University and Hungarian Academy of Sciences, in Budapest, Hungary. For their study, the team described the status of major players within the adaptive and innate immune system in peripheral blood of children with newly diagnosed celiac disease. They then looked to see how the phenotype might have changed once the symptoms improved following treatment with a gluten-free diet. The team drew peripheral blood samples from ten children with biopsy-proven celiac disease at the time of diagnosis and again after once clinical symptoms subsided with treatment by gluten-free diet. They also drew blood samples from a control group of 15 children who suffered from functional abdominal pain. They measured the prevalence of cells of adaptive and innate immunity by means of labeled antibodies against surface markers and intracellular FoxP3 using a flow cytometer. They found that patients with celiac disease had lower T helper, Th1 and natural killer (NK), NKT and invariant NKT cell prevalence and with higher prevalence of activated CD4+ cells, myeloid dendritic cells (DC) and Toll-like receptor (TLR) 2 and TLR-4 positive DCs and monocytes compared to controls. Most of these deviations returned to normal, once symptoms subsided with gluten-free diet treatment. However, prevalence of NK and NKT cell, DC and TLR-2 expressing DCs and monocytes remained abnormal. The immune phenotype in childhood celiac disease indicates that both adaptive and innate immune systems are playing a role in celiac disease. Treatment with a gluten-free diet reverses immune abnormalities, but the mechanics of the reversal likely varies among cell types. Source: Dig Dis Sci. 2010 Aug 5. DOI: 10.1007/s10620-010-1363-6
  10. Celiac.com 04/13/2010 - A team of clinicians recently described a case of immune modulation by non-Hodgkin lymphoma in a patient with two primary intestinal T-Cell lymphomas and long-standing celiac disease. F. Mühr-Wilkenshoff, M. Friedrich, H. D. Foss, M. Hummel, M. Zeitz, and S. Daum made up the research team. They are variously affiliated with the Medical Clinic I, Gastroenterology, Rheumatology and Infectious Diseases, and with the Department of Pathology, Charité of the Campus Benjamin Franklin of University Medicine Berlin, Germany. About 20–30% of all non-Hodgkin lymphomas (NHLs) are gastrointestinal in nature. Of these gastrointestinal lymphomas, about 20–30% occur in small intestine The clinical team recently reported the case of a 72-year-old patient who had been diagnosed with celiac disease when he was 52-years old. The man had not followed a gluten-free diet, yet showed no evidence of enteropathy or celiac-associated antibodies, but still developed a jejunal T-cell lymphoma. Doctors resected the lymphoma due to perforation and treated the patient with four courses of IMVP-16. The patient began and maintained a strict gluten-free diet. Two years later, the patient appeared with weight loss and a clonally divergent refractory sprue type II with loss of antigen (CD8; T-cell receptor-) expression in intraepithelial lymphocytes. At this time, he showed high titers of celiac-associated antibodies, although he was on a strict GFD. The research team notes that the missing enteropathy under a gluten-containing diet supports the idea of immune suppression in malignant diseases, especially non-Hodgkin lymphoma. They also note that the fact that, even while maintaining a strict gluten-free diet, the patient developed refractory sprue type II, an early form of another independent T-cell lymphoma, along with celiac-associated antibodies, suggests that clonal intraepithelial lymphocytes might be stimulating antibody production. Thus, they conclude that isolated detection of celiac-associated antibodies in patients with celiac disease does not prove that patients have deviated from their gluten-free diets. Source: Digestion 2010;81:231–234 DOI: 10.1159/000269810
  11. Celiac.com 03/11/2010 - As part of an effort to investigate the possibility of multiple common variants for celiac disease influencing immune gene expression, a team of more than sixty scientists recently worked together to conduct a second-generation genome-wide association study (GWAS) of 4,533 individuals with clinically proven celiac disease, along with 10,750 control subjects. They genotyped a total of 113 selected SNPs with PGWAS < 10−4 and 18 SNPs from 14 known loci in another 4,918 confirmed celiac disease patients and 5,684 control subjects. The research team included dozens of scientists associated with a variety of major research institutions, hospitals and clinics. The GWAS included five European sample collections of celiac disease and control cases, including the celiac disease dataset reported previously. The team's stringent data quality control measures included calling genotypes using a custom algorithm on both large sample sets and, where possible, cases and controls together. The team tested 292,387 non-HLA SNPs from the Illumina Hap300 marker pool for association in 4,533 individuals with celiac disease and 10,750 control subjects of European descent. They also tested another 231,362 additional non-HLA markers from the Illumina Hap550 marker set for association in a subset of 3,796 individuals with celiac disease and 8,154 controls. All markers came from autosomes or the X chromosome. For both datasets, Genotype call rates were >99.9%. The study showed over-dispersion factor of association test statistics comparable to that observed in other GWASs of this sample size. Factoring in missing genotypes for 737 cases with celiac disease genotyped on the Hap300 BeadChip and corresponding controls did not change the findings in any meaningful way.Variants from 13 new regions reached genome-wide significance (Pcombined < 5 × 10−8); most contain geneswith immune functions, such as BACH2, CCR4, CD80, CIITA-SOCS1-CLEC16A, ICOSLG and ZMIZ1, while ETS1, RUNX3, THEMIS and TNFRSF14 play key roles in thymic T-cell selection. The data suggested associations for 13 additional regions. Expression quantitative trait meta-analysis of 1,469 whole blood samples showed that 52.6% of tested loci (20 of 38 loci) had celiac risk variants corresponding with cis gene expression (P < 0.0028, FDR 5%). Source: Nature Genetics (28 February 2010) | doi:10.1038/ng.543
  12. Celiac.com 11/02/2009 - When it comes to health and wellness, probiotics are the new black. Their role in promoting beneficial gut bacteria and in mediating adverse gut reactions is gaining a great deal of attention and study among the nutrition and health-minded. This is also true in the field of celiac disease research, where the role of probiotic strains in positively influencing various immune reactions within the gut is drawing clinical study and a good deal of interest. A number of strains of probiotic bacteria are important in regulating certain activities in gut-associated lymphoid tissue. By better understanding exactly what factors control probiotic-driven immuno-modulation, researchers hope to improve their role in the treatment, or even prevention, of specific immune-mediated diseases. A team of Italian researchers recently set out to examine the effects of various strains of Lactobacillus spp. and Bifidobacterium lactis in transgenic mice expressing the human DQ8 heterodimer, a HLA molecule linked to celiac disease. The research team was made up of R. D'Arienzo, F. Maurano, P. Lavermicocca, E. Ricca, and M. Rossi of the Institute of Food Sciences, CNR, in Avellino, Italy. The team used live mice mucosally immunized with the gluten component gliadin. To support their efforts, the team conducted in vitro analysis on immature bone marrow-derived dendritic cells (iBMDCs). Their results revealed that all strains up-regulated surface B7-2 (CD86), indicating DC maturation, but with varying intensity. No probiotic strain triggered significant levels of IL-10 or IL-12 in iBMDCs, whereas Lactobacillus paracasei and Lactobacillus fermentum basically induced TNF-alpha expression. Notably, when probiotic bacteria were co-administered in live mice with mucosa immunized with the gluten component gliadin, each of these strains increased the antigen-specific TNF-alpha secretion. The results indicate that probiotics promote strain-specific reactions that support, rather than suppress, the innate and adaptive immune systems of live mice with gluten antigen sensitivity. Using live mice models to better understand the role of probiotic bacteria in mediating immune response to gliadin and other food proteins provides important insight into how such immune responses may be mediated in humans. Such insights will help to speed better treatments for celiac disease and possibly other food-triggered immune reactions. This study supports the notion that Lactobacillus spp. and Bifidobacterium lactis strains may be helpful in promoting better gut health for sufferers of celiac disease. However, further research in humans is needed for conclusive evidence. Source: Cytokine. September 5th, 2009.
  13. Celiac.com 04/10/2006 - This study looks at innate immune response to gliadin. The innate immune system responds to gliadin inducing zonulin release and increasing intestinal permeability and may be a factor in the onset of celiac disease, but I question if this leads ultimately to the Ag-specific adaptive immune response seen in patients with celiac disease. This innate response fails to explain why one identical twin may have celiac disease and not the other. Both of the twins as well as people not even susceptible to celiac disease would presumably have this same innate response to gliadin. I again urge celiac disease researchers to consider gluten-internalizing bacteria as the necessary trigger for the onset of celiac disease. The presence or absence of such bacteria does indeed offer an explanation as to why one twin gets celiac disease and not the other. Zonulin does not. In the commercial supplement product, Glisodin, the properties of gliadin have, in fact, already been used for the last few years to facilitate the delivery of the antioxidant enzyme superoxide dismutase (SOD) protecting it from digestive acids and getting it through the intestinal mucosa, probably taking advantage of the zonulin effect. Aware of celiac disease, the developer of Glisodin tried to use other peptides as a carrier of SOD, but the only gliadin was effective. Unfortunately, this denies celiacs the benefit of using Glisodin to treat oxidative stress. Abstract of Study: J Immunol. 2006 Feb 15;176(4):2512-21. Gliadin Stimulation of Murine Macrophage Inflammatory Gene Expression and Intestinal Permeability Are MyD88-Dependent: Role of the Innate Immune Response in Celiac Disease. Thomas KE, Sapone A, Fasano A, Vogel SN. Department of Microbiology and Immunology. Recent studies have demonstrated the importance of TLR signaling in intestinal homeostasis. Celiac disease (celiac disease) is an autoimmune enteropathy triggered in susceptible individuals by the ingestion of gliadin-containing grains. In this study, we sought to test the hypothesis that gliadin initiates this response by stimulating the innate immune response to increase intestinal permeability and by up-regulating macrophage proinflammatory gene expression and cytokine production. To this end, intestinal permeability and the release of zonulin (an endogenous mediator of gut permeability) in vitro, as well as proinflammatory gene expression and cytokine release by primary murine macrophage cultures, were measured. Gliadin and its peptide derivatives, 33-mer and p31-43, were found to be potent inducers of both a zonulin-dependent increase in intestinal permeability and macrophage proinflammatory gene expression and cytokine secretion. Gliadin-induced zonulin release, increased intestinal permeability, and cytokine production were dependent on myeloid differentiation factor 88 (MyD88), a key adapter molecule in the TLR/IL-1R signaling pathways, but were neither TLR2- nor TLR4-dependent. Our data support the following model for the innate immune response to gliadin in the initiation of celiac disease. Gliadin interaction with the intestinal epithelium increases intestinal permeability through the MyD88-dependent release of zonulin that, in turn, enables paracellular translocation of gliadin and its subsequent interaction with macrophages within the intestinal submucosa. There, the interaction of gliadin with macrophages elicits a MyD88-dependent proinflammatory cytokine milieu that facilitates the interaction of T cells with APCs, leading ultimately to the Ag-specific adaptive immune response seen in patients with celiac disease.
  14. Celiac.com 09/25/2009 - Scientists at the Ottawa Hospital Research Institute and the University of Ottawa have uncovered what looks to be an important clue regarding the causes of type 1 diabetes. A research team led by Dr. Fraser Scott recently screened 42 patients with type 1 diabetes and found that nearly half showed an abnormal immune response to wheat proteins. Dr. Scott is a Senior Scientist at the Ottawa Hospital Research Institute and Professor of Medicine at the University of Ottawa. The research team includes Dr. Majid Mojibian, Dr. Habiba Chakir, Dr. David E. Lefebvre, Jennifer A. Crookshank, Brigitte Sonier and Dr. Erin Keely. In most people, the immune system functions normally, identifying and attacking dangerous foreign visitors, like viruses and bacteria, without harming healthy body tissue or other benign molecules, including food molecules in the digestive tract. The breakdown of this process contributes to the development of various autoimmune diseases and allergies. In the case of Type 1 diabetes, the immune system wrongly targets the cells of the pancreas, the organ responsible for regulation of blood sugar. Globally, diabetes afflicts nearly 250 million people. Type 1 diabetes, the most severe form of the disease, makes up about 10 percent, or about 25 million, of that worldwide total. There is currently no cure for Type 1 diabetes, and sufferers require daily insulin injections can help control blood sugar levels. Dr. Scott’s results offer the first suggestions that T cells in the immune systems of type 1 diabetics are also more likely to have adverse immune reactions to wheat. His results also suggest that such over-reaction is tied to genes associated with type 1 diabetes. According to Dr. Scott, the research suggests that "people with certain genes may be more likely to develop an over-reaction to wheat and possibly other foods in the gut and this may tip the balance with the immune system and make the body more likely to develop other immune problems, such as type 1 diabetes.” Dr. Scott adds that the immune system has to find "the perfect balance to defend the bodyagainst foreign invaders without hurting itself or over-reacting to theenvironment and this can be particularly challenging in the gut, wherethere is an abundance of food and bacteria.” In side comments that accompany the paper, diabetes expert Dr. Mikael Knip of Finland suggest that the team's results "add to the accumulating concept that the gut is an active player in the diabetes disease process.” Earlier animal models studies by Dr. Scott have shown that a wheat-free diet can reduce the risk of developing diabetes, but he notes that more research is needed to confirm the association and to assess possible effects of diet changes in humans. More research is also needed to examine possible connections to celiac disease, an autoimmune disease associated with adverse immune reactions to wheat proteins that has significant associations with diabetes. This research project was funded by the Juvenile Diabetes Research Foundation and the Canadian Institutes of Health Research. Source: Diabetes - August 2009
  15. A team of Swiss researchers recently set out to examine the nature of T cell-mediated immuno-regulation in the gastrointestinal tract. The research team was made up of doctors L. Saurer and C. Mueller of the Institute of Pathology at the University of Bern in Switzerland. In the human intestinal tract, just a single layer of epithelial cells divides innate and adaptive immune effector cells from a wide array of antigens. Here, the immune system faces a tall task in accepting beneficial flora and dietary antigens while preventing the dissemination of potential pathogens. When the tightly controlled process of immune system reactions breaks down, harmful inflammation and damage may result. In light of this, a great deal of focus has shifted toward 'conventional' regulatory CD4+ T cells, including naturally occurring and adaptive CD4+ CD25+ Foxp3+ T cells, Th3 and Tr1 cells. However, control mechanisms in the intestinal mucosa are highly intricate, and include adaptations of non-haematopoietic cells and innate immune cells in addition to the presence of unconventional T cells with regulatory properties such as resident TCRγδ or TCRαβ CD8+ intraepithelial lymphocytes. In the study, L. Saurer and C. Mueller seek to provide an overview of the present body of knowledge on standard and non-standard regulatory T cell subsets (Tregs), with particular focus on clinical data and the potential role or malfunctioning of Tregs in four major human gastrointestinal diseases, i.e. inflammatory bowel diseases, celiac disease, food allergy and colorectal cancer. Their data confirms most of the findings derived from experimental animal models, and has implications for clinical immunology, food allergy, immunoregulation, immunotherapy, mucosal immunology, and regulatory T cell protocols. Their findings appear in the February 2009 issue of Allergy.
  16. Nature Immunology 2, 353 - 360 (April 2001) Celiac.com 04/12/2001 - According to an article published in the April issue of Nature Immunology, Dr. Marc Rothenberg and colleagues at the Childrens Hospital Medical Center in Cincinnati, Ohio performed a series of experiments on mice which led them to the conclusion that white blood cells called eosinophils could be the cause of many food allergies and gastrointestinal inflammation. The researchers believe that the eosinophil cells, which are present throughout the body, mistakenly identify food proteins as germs in individuals with food allergies. When the intestinal lining of an allergic person is exposed to an allergen, a substance called eotaxin is released by the cells lining the intestine, which causes the eosinophil cells and other immune cells to attack them and release powerful proteins that destroy the surrounding tissues and cause eosinophilic inflammation. The results of this study are unique because this is the first time eosinophils cells have been implicated in causing allergies, even though scientists have known for some time that they were present in great numbers at the sites of inflammation caused by reactions to food. The implication of this study is the possible development of drugs that stop this reaction from occurring, and thus prevent digestive inflammation and destruction that occurs when people with food allergies eat foods to which they are allergic. These results put scientists one step further in understanding how and why the digestive system is attacked in certain individuals, and a possible means of one day controlling the process.