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Celiac.com 06/14/2023 - Researchers from Lanzhou University in China, in collaboration with international scientists, say they have developed a promising new method for treating celiac disease. Led by Aman Khan, a Pakistani postdoctoral fellow at Lanzhou University, the team focused on isolating probiotic bacterial strains from Pakistani fermented sourdough bread to prevent the occurrence of celiac disease. Celiac disease is an immune disorder triggered by gluten consumption and is particularly prevalent in Asian countries like Pakistan, where diets high in gluten-containing foods are common. Khan aimed to leverage his expertise to aid those affected by this condition. Inspired by a previous study that isolated a probiotic strain from a traditional Chinese fermented food called jiangshui, which showed the ability to degrade uric acid and regulate gut microbiota, Khan and his team sought to isolate beneficial strains from Pakistani fermented sourdough bread. They successfully extracted probiotic bacterial strains called LZU-GM and conducted experiments on mice. Probiotics from Fermented Sourdough The results of their experiments and integrative analysis indicated that LZU-GM could mitigate the adverse effects of gluten additives in food and restore balance to gut microbiota in mice. However, further clinical trials are required to evaluate the safety and efficacy of these probiotics from fermented sourdough bread as a potential treatment for celiac disease. The team plans to continue their research by creating yogurt using the LZU-GM strains isolated from Pakistani sourdough bread and conducting additional experiments. Their goal is to develop a therapeutic adjunct agent that can be used in conjunction with existing treatments for celiac disease. The researchers believe their innovative solution holds promise for individuals living with this autoimmune disorder. Big Claims But Few Details While the researchers claim to have developed a promising new method for treating celiac disease, it is important to approach their findings with caution. The study focused on isolating probiotic bacterial strains from Pakistani fermented sourdough bread, aiming to prevent the occurrence of celiac disease. The results of experiments conducted on mice showed potential benefits, including the mitigation of adverse effects of gluten additives and restoration of gut microbiota balance. However, it is crucial to note that these findings are based on animal studies, and further clinical trials are necessary to assess the safety and efficacy of these probiotics in treating celiac disease in humans. More Evidence Needed Big claims require robust evidence, and at this stage, the evidence supporting the use of probiotic strains from fermented sourdough bread as a treatment for celiac disease is limited. While the preliminary results sound promising, it is important to emphasize the need for rigorous scientific investigation, including well-designed clinical trials, to validate the potential of these probiotics. Until conclusive evidence emerges from rigorous clinical trials, it is essential to remain cautious and prioritize thorough scientific scrutiny before considering these probiotics as a viable treatment option for individuals living with celiac disease. Read more in chinadaily.com
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Celiac.com 02/04/2014 - According to a new article by a team of researchers, not all gluten protein is created equal. That is, not all gluten proteins trigger an immune response in people with celiac disease. The research team included Elma M.J. Salentijn, Danny G. Esselink, Svetlana V. Goryunova, Ingrid M. van der Meer, Luud J.W.J. Gilissen, and Marinus J.M. Smulders. They are variously affiliated with the Plant Research International in Wageningen, The Netherlands, and the Vavilov Institute of General Genetics at the Russian Academy of Sciences in Moscow, Russia. Gluten proteins are the source of peptides that can trigger a T cell reaction in celiac disease patients, leading to inflammatory responses in the small intestine. Various peptides with three major T cell epitopes involved in celiac disease are derived from alpha-gliadin fraction of gluten. Numerous factors are known to influence the immunogenicity of individual gene family members, as alpha-gliadins are encoded by a large multi-gene family and amino acid variation in the celiac disease epitopes. That means that some wheat strains are more likely to trigger celiac disease, and other are less likely. Current commercial methods of gluten detection cannot tell the difference between immunogenic and non-immunogenic celiac epitope variants, and thus cannot accurately measure the overall celiac epitope load of a given wheat strain. Being able to tell the difference between what types of wheat have a lower likelihood to cause or trigger celiac disease is important to commercial wheat growers and producers. The team developed a 454 RNA-amplicon sequencing method for alpha-gliadin transcripts that includes the three major celiac disease epitopes and their variants. They used the method to screen 61 different durum wheat cultivars and accessions. They found a total of 304 unique alpha-gliadin transcripts, corresponding to a total of 171 ‘unique deduced protein fragments’ of alpha-gliadins. They used the numbers of these fragments obtained in each plant to calculate quantitative and quantitative differences between the celiac epitopes expressed in the endosperm of these wheat plants. A small number of wheat plants showed a lower ratios of celiac epitope-encoding alpha-gliadin transcripts, though none were entirely free of celiac epitopes. Dedicated 454 RNA-amplicon sequencing allows researchers to group wheat plants according to the genetic variation in alpha-gliadin transcripts, and to screen for plants which are potentially less likely to trigger or promote celiac disease. The alpha-gliadin sequence database the team constructed will provide an important reference in proteomics analysis regarding the immunogenic potential of mature wheat grains. Source: BMC Genomics 2013, 14:905. doi:10.1186/1471-2164-14-905
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Celiac.com 04/12/2017 - Researchers at Hiroshima University say they have perfected the science behind a new bread-baking recipe. Developed by Japan's National Agriculture and Food Research Organization, NARO, the method uses rice-flour to produce gluten-free bread with a similar consistency and volume to traditional wheat-flour loaves. Now, rice-flour based gluten-free breads are old hat, but they've long had a reputation for being dry, crumbly, soulless creations that pale in comparison to even the cheapest traditional breads. The Japanese rice bread is 100% natural, and offers a consistency and texture similar to wheat breads. Breads made with wheat flour are soft, spongy and chewy in large part because of gluten's ability to form a flexible matrix. This matrix provides stability for the thin dough/bread walls, which are formed between CO2 bubbles produced by fermenting yeast. It also enables bread to "rise" in response to increasing CO2 levels during the baking process. Since standard rice flour contains no gluten, the researchers needed to develop a new method that would bring these vital bread characteristics to their gluten-free bread. NARO solved the problem by using a specific type of wet milling process to produce their rice flour. The wet-mill process to make flour for gluten-free bread permits the formation of a microstructure of the fermenting batter, and in the resulting loaf, creating tiny bubbles coated in uniform undamaged starch particles in suitably supportive matrix. The research team found that this process created properties previously unseen in rice-flour; properties arising from the undamaged starch particles created by the milling technique They dub this supportive matrix "stone walls,” and they apparently form due to the surface activity of the undamaged starch granules. It appears these granules are able to lower the surface tension of water, and reduce the likelihood of collapse in the formed bubble walls. The result is spongier, chewier bread. Some of the researchers suspect that the stability of the undamaged starch bubble is due to the uniform hydrophobicity of the similar sized granules, and that these cause an interface between damp gaseous air pockets and the liquid batter. Whatever the exact reason, this "stone wall" matrix allows bubbles to grow and expand as interior CO2 levels increase, which leads to superior bread loaves. This technique has the potential to revolutionize the gluten-free bread industry. Stay tuned to see how the story evolves. Source: Sciencedaily.com
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Celiac.com 03/17/2014 - Researchers know a great deal about the function of human digestive proteases in gluten proteins, but they know very little about the role of intestinal microbes in metabolizing those proteins. A team of researchers recently set out to examine the isolation and characterization of human gut bacteria involved in the metabolizing gluten proteins. The researchers include Alberto Caminero, Alexandra R. Herrán, Esther Nistal, Jenifer Pérez-Andrés, Luis Vaquero, Santiago Vivas, José María G. Ruiz de Morales, Silvia M. Albillos, and Javier Casqueiro. They are variously affiliated with the Instituto de Biología Molecular, Genómica y Proteómica (INBIOMIC), and the Instituto de Biomedicina (IBIOMED) at the Campus de Vegazana of the Universidad de León, with the Área de Microbiología, Facultad de Biología y Ciencias Ambientales at the Universidad de León, with the Departamento de Inmunología y Gastroenterología, Hospital de León, León, Spain, and with the Instituto de Biotecnología (INBIOTEC) de León, all in León, Spain. For their study, the team cultured 22 human fecal samples, with gluten as the principal nitrogen source, and isolated 144 strains belonging to 35 bacterial species that may play a role in gluten metabolism in the human gut. They found that 94 of the isolated strains were able to metabolize gluten, 61 strains showed an extracellular proteolytic activity against gluten proteins, while several strains showed a peptidasic activity toward the 33-mer peptide, which is an known peptide trigger in celiac disease patients. Most of the isolated strains belong to the phyla Firmicutes and Actinobacteria, mainly from the genera Lactobacillus, Streptococcus, Staphylococcus, Clostridium and Bifidobacterium. They found that the human gut hosts a wide variety of bacteria capable of using gluten proteins and peptides as nutrients. These bacteria could play an important role in gluten metabolism and could offer promising new treatment possibilities for celiac disease. Source: Onlinelibrary.wiley.com. DOI: 10.1111/1574-6941.12295
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Celiac.com 10/25/2017 - For people with celiac disease, eating gluten proteins from wheat, barley, and rye triggers an auto-immune response, and the accompanying physical symptoms. A team of researchers recently set out to engineer low-gluten wheat strains that also have low-reactivity for people with celiac disease. To meet their goals, the team designed two sgRNAs to target a conserved region adjacent to the coding sequence for the 33-mer in the -gliadin genes. They then sought to evaluate the results. The research team included Susana Sánchez-León, Javier Gil-Humanes, Carmen V. Ozuna, María J. Giménez, Carolina Sousa, Daniel F. Voytas, and Francisco Barro. They are variously affiliated with the Departamento de Mejora Genética Vegetal, Instituto de Agricultura Sostenible (IAS-CSIC), Córdoba, Spain; the Department of Genetics, Cell Biology, and Development, Center for Genome Engineering at the University of Minnesota in Minneapolis, MN, USA; and with the Facultad de Farmacia, Departamento de Microbiología y Parasitología, Universidad de Sevilla, Spain. The gliadin gene family of wheat includes four highly reactive peptides, with the 33-mer peptide being the main culprit in celiac patients. In all, the team generated twenty-one mutant lines, all of which showed strong reduction gliadin proteins. Of the 45 different genes identified in wild type gliadin, the team mutated up to 35 different genes in one of the lines to achieve an 85% reduction in immunoreactivity. They then identified the transgene-free lines, and found no off-target mutations in any of the potential targets. So, what does this all mean in English? Well, basically the low-gluten, transgene-free wheat lines that the team describes here could be used to produce low-gluten foods, as well as serving as source material to introduce the low-gluten, low-reactivity traits into selected wheat varieties. Basically, the technology could be used to create low-gluten wheat varieties with low immunoreactivity. Now, most folks with celiac disease, especially those with higher gluten sensitivity, would likely need more than and 85% reduction in immunoreactivity to see any real benefit. However, this study provides an interesting glimpse at how science might help researchers to create wheat strains that are safe for people with celiac disease. Source: Plant Biotechnology Journal. DOI: 10.1111/pbi.12837
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Celiac.com 06/15/2017 - Enteropathy-associated T cell lymphoma (EATL) subtypes are characterized by loss of function of SETD2. Although EATL is rare condition, it is deadly. It is also the most common neoplastic complication of celiac disease. A team of researchers recently conducted whole-exome sequencing of 69 EATL tumors, which helped them to define the genetic landscape of EATL. They found that SETD2 was silenced in 32% of EATL patients, making it the most frequently silenced gene in EATL. The research team included AB Moffitt, SL Ondrejka, M McKinney, RE Rempel, JR Goodlad, CH Teh, S Leppa, S Mannisto, PE Kovanen, E Tse, RKH Au-Yeung, YL Kwong, G Srivastava, J Iqbal, J Yu, K Naresh, D Villa, RD Gascoyne, J Said, MB Czader, A Chadburn, KL Richards, D Rajagopalan, NS Davis, EC Smith, BC Palus, TJ Tzeng, JA Healy, PL Lugar, J Datta, C Love, S Levy, DB Dunson, Y Zhuang, ED Hsi, and SS Dave. The team also noted that the JAK-STAT pathway was the most frequently mutated pathway, with frequent mutations in STAT5B as well as JAK1, JAK3, STAT3, and SOCS1, and that the condition causes highly overlapping genetic alterations among the mutations in KRAS, TP53, and TERT Type I EATL and type II EATL (monomorphic epitheliotropic intestinal T cell lymphoma), which indicates shared mechanisms underlying their causes. To model the effects of SETD2 loss in vivo, the team developed a T cell-specific knockout mouse. These mice manifested an expansion of γδ T cells, indicating novel roles for SETD2 in T cell development and lymphomagenesis. The team's data provides the most comprehensive genetic portrait to date of this rare, but deadly disease, and will likely play a key role in future classifications of EATL. Source: J Exp Med. 2017 May 1;214(5):1371-1386. doi: 10.1084/jem.20160894. Epub 2017 Apr 19. The researchers are variously affiliated with the Duke Center for Genomics and Computational Biology, Duke University, Durham, NC, the Duke Cancer Institute, Duke University School of Medicine, Durham, NC, the Pathology and Laboratory Medicine Institute, Cleveland Clinic, Cleveland, OH, the Haematological Malignancy Diagnostic Service, St. James's University Hospital, Leeds LS9 7TF, England, UK, the Haematology Department, Western General Hospital, Edinburgh, Scotland, UK, the Department of Oncology and Research Program Unit, Faculty of Medicine, Helsinki University Hospital Cancer Center and University of Helsinki in Helsinki, Finland, HUSLAB and Medicum, Helsinki University Hospital Cancer Center and University of Helsinki, Helsinki, Finland, the University of Hong Kong, Queen Mary Hospital, Hong Kong, China, the University of Nebraska Medical Center, Omaha, NE, Imperial College London, London, England, UK, the British Columbia Cancer Agency, University of British Columbia, Vancouver, BC, Canada, the University of California, Los Angeles, Los Angeles, CA, Indiana University, Indianapolis, IN, the Presbyterian Hospital, Pathology and Cell Biology, Cornell University, New York, NY, the University of North Carolina at Chapel Hill, Chapel Hill, NC, the Department of Medicine, Duke University School of Medicine, Durham, NC, the Department of Statistical Science, Duke University, Durham, NC, the Hudson Alpha Institute for Biotechnology, Huntsville, AL 35806, and the Department of Immunology, Duke University School of Medicine, Durham, NC.
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Want to Help Catalog, Track Autoimmune Diseases?
Jefferson Adams posted an article in Additional Concerns
Celiac.com 03/18/2017 - Do you have an autoimmune disease? Does someone you know? Did you know that the numbers regarding autoimmune rates are all over the place, and that incomplete or wrong information can result in delayed or missed diagnoses? Want to help researchers create a database that will help them understand exactly how many people are living with autoimmune conditions? Then behold the latest project from ARI, a 501c(3) nonprofit, with a mission "to create a hub for research, statistics, and patient data on all autoimmune illnesses." The project seeks to provide data that will help researchers nail down some basic answers about the numbers of people who live with one or more autoimmune conditions. The ARI website says that the company "operate a national database for patients who suffer from any autoimmune disease." ARI's mission is to "reduce the time of diagnosis, support research, compute prevalence statistics, and establish autoimmune disease as a major class of disease so that it receives the awareness of the public, the attention of healthcare providers, and the appropriate funding needed to improve upon existing treatment protocols and disease management strategies." This is one reason why Aaron Abend, the founder and president of ARI, decided to create the Autoimmune Registry after his mother was misdiagnosed for 10 years because, based on incorrect statistical data, "doctors thought Sjogren's syndrome was a rare disease with only 37,000 cases in the U.S." Today, researchers agree there are probably 3 million cases in the U.S., so not so rare at all. Researchers currently estimate that anywhere from 9 million to 50 million people in the United States have an autoimmune disease. That's quite a wide range. Pinpointing the actual prevalence is part of what ARI will try to do. So, they are reaching out directly to patients to information about diseases like rheumatoid arthritis (RA), lupus, psoriasis, diabetes, Crohn's, celiac disease, Sjogren's syndrome, multiple sclerosis (MS), and many others fall under the autoimmune umbrella. The registry is easy to join. It is free to sign up and consists of a simple survey that people with autoimmune diseases answer. The information that people provide to ARI remains secure. The data may be used to compile statistics and qualify them for research opportunities, but no identifying information will be shared without permission. The hope is that the registry can help researchers connect with people and the data. You can view the registry here.-
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Celiac.com 12/26/2016 - Could gluten-degrading enzymes offer a better future for celiac patients? Rothia mucilaginosa is an oral microbial colonizer that can break down proline- and glutamine-rich proteins present in wheat, barley, and rye that contain the immunogenic sequences that drive celiac disease. A team of researchers recently set out to isolate and identify the enzymes and evaluate their potential as novel enzyme therapeutics for celiac disease. The research team included G Wei, N Tian, R Siezen, D Schuppan, and EJ Helmerhorst. They are variously affiliated with the Department of Molecular and Cell Biology at the Henry M. Goldman School of Dental Medicine in Boston, Massachusetts; the Bacterial Genomics Group, Center for Molecular and Biomolecular Informatics at Radboud University Medical Centre, Nijmegen, the Netherlands; the Division of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts; and with the Institute of Translational Immunology and Research Center for Immunology, University Medical Center, Johannes-Gutenberg-University, Mainz, Germany. They first extracted and separated membrane-associated R. mucilaginosa proteins using DEAE chromatography. They tracked enzyme activities using paranitroanilide-derivatized and fluorescence resonance energy transfer (FRET) peptide substrates, and by gliadin zymography. They determined epitope elimination in R5 and G12 ELISAs. They identified gliadin-degrading Rothia enzymes by LC-ESI-MS/MS as hypothetical proteins ROTMU0001_0241 (C6R5V9_9MICC), ROTMU0001_0243 (C6R5W1_9MICC), and ROTMU0001_240 (C6R5V8_9MICC). The Rothia subtilisins and two subtilisins from Bacillus licheniformis, subtilisin A and the food-grade Nattokinase, efficiently degraded the immunogenic gliadin-derived 33-mer peptide and the immunodominant epitopes recognized by the R5 and G12 antibodies. This study identified Rothia and food-grade Bacillus subtilisins as promising new candidates for enzyme therapeutics in celiac disease. To do this, the team cleaved succinyl-Ala-Ala-Pro-Phe-paranitroanilide, a substrate for subtilisin with Pro in the P2 position, as in Tyr-Pro-Gln and Leu-Pro-Tyr in gluten, which are also cleaved. Consistently, FRET substrates of gliadin immunogenic epitopes comprising Xaa-Pro-Xaa motives were rapidly hydrolyzed. They found that Rothia subtilisins and two subtilisins from Bacillus licheniformis, subtilisin A and the food-grade Nattokinase, efficiently degraded the immunogenic gliadin-derived 33-mer peptide and the immunodominant epitopes recognized by the R5 and G12 antibodies. Rothia and food-grade Bacillus subtilisins show promise for development as enzyme therapies for celiac disease. Source: Am J Physiol Gastrointest Liver Physiol. 2016 Sep 1;311(3):G571-80. doi: 10.1152/ajpgi.00185.2016. Epub 2016 Jul 28
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Celiac.com 10/24/2016 - A team of researchers led by Mahmoud A Ghannoum, PhD, professor and director of the Center for Medical Mycology at Case Western Reserve and University Hospitals Cleveland Medical Center, has made a breakthrough in understanding Crohn's disease. The researchers were the first to document the role of a fungus in the human gut as playing a major role in Crohn's disease. As part of their efforts, their research team assessed the mycobiome and bacteriome of patients with Crohn's disease, their Crohn's-free first degree relatives in 9 families in northern France and Belgium, and in Crohn's-free individuals from 4 families in the same region. For their study, the team analyzed fecal samples from 20 Crohn's patients, and from 28 Crohn's-free patients from nine families, and of 21 Crohn's-free patients from four nearby families. The team found that people with Crohn's disease showed strong fungal-bacterial interaction. Specifically, in Crohn's, two bacteria, Escherichia coli and Serratia marcescens, acted in unison with the fungus Candida tropicalis. Family members with Crohn's showed substantially higher numbers of all three microbes, as compared to their healthy relatives, suggesting co-action between the bacteria and fungus in the gut. The team's lab tests confirmed that the three work together by E. coli cells fusing to the fungal cells, while S. marcescens acts as a bridge to connect the microbes. This produces what is called a biofilm, a thin, slimy layer of microorganisms that, among other things, coats part of the intestinal tract, triggering the inflammation seen in Crohn's disease. Researchers had previously found the fungus in mice with Crohn's, but this is the first time any fungus has been linked to Crohn's in humans. The study is also the first to document S. marcescens as a main factor in Crohn's. The team also found that Crohn's patients suffer from substantially reduced numbers of beneficial bacteria, which corroborated earlier study findings. These findings could lead to helpful new treatment approaches to the traditionally stubborn condition that is Crohn's disease. Source: ScienceDaily.com
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German Researchers Chase Causes of Wheat Sensitivities
Jefferson Adams posted an article in Latest Research
Celiac.com 07/01/2016 - Between five to ten percent of Germans may suffer from wheat intolerance. These people suffer immune reactions when they eat wheat and other cereals such as spelt, rye, and barley. They suffer symptoms including diarrhea, fatigue, psychological disorders, and worsening of chronic inflammatory diseases. They may have celiac disease, wheat allergy, and non-celiac-non allergy wheat sensitivity (NCWS). Now doctors and biomedical and agricultural researchers at Johannes Gutenberg University Mainz (JGU) and the University of Hohenheim have joined forces to study these disorders, especially NCWS. They are gearing their research towards the breeding of new types of wheat that lack these disease causing properties, while maintaining favorable characteristics, such as good baking properties and palatability. The researchers have three main aims. Firstly, they want to find out how the content of wheat proteins called alpha-amylase-trypsin inhibitors (ATI's) has naturally evolved in the various wheat varieties. For this purpose, they are looking at whether there are differences in ATI content in older and newer varieties, the extent to which this is genetically determined in each variety, and whether environmental influences play a role. They also hope to establish exactly how many proteins belong to the family of ATIs in the wheat varieties examined and which of these proteins mainly cause the immune response. The harvested samples are thus being analyzed for ATI content by genetic and proteome methods, while human cell lines are being used to evaluate their immune system-activating effects in the laboratory. Lastly, the scientists hope to be able to establish how far ATI content affects baking properties and palatability, evaluating the wheat variants on the basis of standard quality criteria. Finally, and outside of the current proposal, "we plan several proof-of-concept clinical studies with patients that suffer from defined chronic diseases to assess how far a significant reduction of ATIs in the diet, for example by approximately 90 percent, may improve their condition," said Schuppan. The goal over the medium term is to use the findings to breed new varieties of wheat that sensitive population groups will better tolerate. "We thus need to get the balance correct and create wheat varieties with a low ATI content that still have good baking properties and palatability," concluded Longin. Source: eurekalert.org.- 3 comments
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Celiac.com 04/23/2015 - It's well-known that many people with celiac disease experience neuropathy and other nerve disorders. Now, a team of Israeli researchers are cautiously proposing a link between gluten reactions and ALS. The research team, from the Tel Aviv Medical Center, believes that the gluten sensitivity seen in people with celiac disease might have a connection with ALS, or amyotrophic lateral sclerosis. Their study linking tissue transglutaminase 6 antibodies to ALS is the first study to document a connection between ALS and antibodies to a particular enzyme. Also known as Lou Gehrig's disease, ALS is a progressive disease that attacks nerve cells and pathways in the brain and spinal cord, eventually causing paralysis. In the study, researcher Vivian Drory and her team found antibodies to an enzyme produced in the brain, called tissue transglutaminase 6 (TG6), in 23 out of 150 patients with ALS, but in only five of 115 healthy volunteer subjects. Furthermore, ALS patients showed higher concentrations of those antibodies. It's well documented that people with celiac disease produce antibodies to another transglutaminase, TG2, when they eat gluten, a protein in wheat, barley and rye. Interestingly, nearly half (45%) of patients with celiac disease also produce antibodies to TG6, even when they have no neurological symptoms. Droury's team set out to evaluate the prevalence of celiac disease-related antibodies and HLA antigen alleles, as well as TG6 antibodies, in patients with ALS and healthy individuals serving as controls to determine whether a neurologic presentation of a gluten-related disorder mimicking ALS might occur in some patients. They conducted a case-control study in an ALS tertiary center, where they measured serum levels of total IgA antibodies, IgA antibodies to transglutaminase 2 (TG2) and endomysium, along with IgA and IgG antibodies to deamidated gliadine peptide and TG6 and performed HLA antigen genotyping in 150 consecutive patients with ALS and 115 healthy volunteers of similar age and sex. Study subjects did not have any known autoimmune or gastroenterologic disorder, and none was receiving any immunomodulatory medications. The team found that ALS patients with antibodies to TG6 showed the classic picture of ALS and the typical rate of disease progression. The volunteers with antibodies to TG6 showed no signs of any disease. All patients and control group participants were seronegative to IgA antibodies to TG2, endomysium, and deamidated gliadine peptide. Twenty-three patients (15.3%) were seropositive to TG6 IgA antibodies as opposed to only 5 controls (4.3%) (P = .004). The patients seropositive for TG6 showed a classic picture of ALS, similar to that of seronegative patients. The team tested fifty patients and 20 controls for celiac disease-specific HLA antigen alleles; 13 of 22 TG6 IgA seropositive individuals (59.1%) tested seropositive for celiac disease-related alleles compared with 8 (28.6%) of the 28 seronegative individuals (P = .04). Average levels of IgA antibodies to TG6 were 29.3 (30.1) in patients and 21.0 (27.4) in controls (P = .02; normal, <26). Average levels of IgA antibodies to TG2 were 1.78 (0.73) in patients and 1.58 (0.68) in controls (normal, <10). In a subset of study participants, mean levels of deamidated gliadin peptide autoantibodies were 7.46 (6.92) in patients and 6.08 (3.90) in controls (normal, <16). None of the ALS patients or volunteers had the antibodies to TG2 that are commonly associated with celiac disease, but the ALS patients were more likely to show the genetic mutations that put them at risk for celiac disease. Drory said her team has begun to study TG6 antibody levels in patients newly diagnosed with ALS, and they will be testing the effects of a gluten-free diet in some of those that test positive. However, theirs is just one report, and Drory expects it will be at least a couple of years before the team has any solid results. Her team is also inviting further input from other centers, and study of their data. In the meantime, she warns ALS patients against adopting a gluten-free diet without "clear evidence of antibodies," because any imbalance of diet might prove harmful. It's also worth remembering that an association is not the same as a cause. At least one earlier study concluded that there was no association between TG6 antibodies and either neurological disease or gluten itself. The possibility of a link between celiac disease and a degenerative nerve disease like ALS is interesting, to say the least. The findings of this team will likely invite more examination of any connection between gluten reactions and nerve disorders, so stay tuned for any follow-up news. Source: JAMA Neurol. 2015 Apr 13. doi: 10.1001/jamaneurol.2015.48.
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Celiac.com 01/13/2016 - Researchers are zeroing in on markers for gluten sensitivity in people who don't have celiac disease. So far, there's been scant proof of what causes gluten sensitivity in people who don't have celiac disease. It's been difficult to even pin down the existence of a condition that can be tested and diagnosed. The results of a recent study may change that. The study, from Giovanni Barbara and his team at the University of Bologna, Italy, suggests that inflammation in gluten-sensitive individuals may result from high levels of a molecule called zonulin. Zonulin has been linked to inflammation, and people with celiac disease have been shown to have high levels of zonulin when consuming wheat protein. Symptoms include abdominal pain, bloating, alternating diarrhea or constipation. And there can be other symptoms, including "brain fog," headache, fatigue and joint and muscle pain. Barbara's study found that zonulin levels in gluten-sensitive individuals almost matched those of celiacs. The researchers stress the preliminary nature of the results, but note that this information could lead to testing methods for detecting gluten sensitivity in people who don't have celiac disease. According to gastroenterologist Alessio Fasano of Massachusetts General Hospital in Boston, about 6 percent of the global population may be sensitive to gluten, so any breakthrough in identifying and testing for non-celiac gluten sensitivity could impact tens of millions of people worldwide. Stay tuned for more on zonulin and it's role in non-celiac gluten sensitivity. Source: NPR.ORG
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Celiac.com 12/02/2015 - A strict gluten-free diet remains the only effective treatment for celiac disease, but studies of gluten-free diet adherence have rarely used precise means of measuring data, which means that there really hasn't been much good data on long-term adherence to the gluten-free diet in the adult population. So, what are the factors that keep people on a gluten-free diet? This question has been on the minds of numerous celiac disease researchers. To determine the long-term adherence to the gluten-free diet and potential associated factors, a research team recently conducted a survey of adult celiac patients in a large celiac disease referral center population. The research team included J. Villafuerte-Galvez; R. R. Vanga; M. Dennis; J. Hansen; D. A. Leffler; C. P. Kelly; and R. Mukherjee. They are variously affiliated with the Celiac Center, Division of Gastroenterology, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA. Their team performed a mail survey of adults with clinically, serologically and histologically confirmed celiac disease diagnosed five or more years prior to the survey. To measure dietary adherence, the team used the previously validated Celiac Disease Adherence Test. The team then analyzed demographic, socio-economic and potentially associated factors as they relate to dietary adherence. Of 709 people surveyed, about half responded. Their responses showed an average of about 10 years on a gluten-free diet, plus or minus 6.4 years. Adequate adherence was measured by a celiac disease adherence test score under 13. Just over 75% of respondents reported adequate dietary adherence. A higher level of education was associated with adequate adherence (P = 0.002) even after controlling for household income (P = 0.0220). Perceptions of cost, effectiveness of the gluten-free diet, knowledge of the gluten-free diet and self-effectiveness at following the gluten-free diet correlated with adherence scores (P < 0.001). More than 75% of respondents reported long-term adherence to a gluten-free diet Perceived cost remains one of the main barriers to long-term adherence to a gluten-free diet. Perceptions of effectiveness of gluten-free diet as well as its knowledge, are potential areas where better information may increase dietary compliance. Source: Aliment Pharmacol Ther. 2015;42(6):753-760.
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Celiac.com 07/01/2015 - Children with celiac disease show an impaired immune response to the hepatitis B vaccine, and neither a gluten-free diet, nor additional vaccine boosters seem to change that, according to research presented at the 33rd Annual Meeting of the European Society for Paediatric Infectious Diseases. Although a number of studies have documented this reduced response, most have been limited by low numbers of patients with celiac disease, and/or lower numbers of control patients, said Maria José Pérez, MD, from Henares Hospital in Coslada, Spain. Two of those prior studies that implicated gluten in the impaired vaccine response, showed that celiac patients who follow a gluten-free diet have a hepatitis B vaccine response that is similar to that in the general population after celiac patients switch to a gluten-free diet. In their study, Dr. Pérez and her colleagues looked at the immune response to the vaccine in children with celiac disease. The team evaluated 214 children with celiac disease and 346 control patients who had completed the hepatitis B vaccine regimen in the first year of life. All patients were vaccinated before gluten was introduced into their diets. They measured gluten antibody levels for each child to determine vaccine response. Kids who showed levels of hepatitis B surface antibody under 10 mUI/mL were defined as non-responsive to the vaccine. Overall, non-response was 8% higher in children with celiac disease than in control subjects (68.7% vs 60.7%). For children younger than 5 years, this difference was a whopping 20%, with a rate of 50.0% for celiac children, compared with 30.1% for the control group (P = .015). In children with celiac disease, the researchers found no relation between level of antibody and time since the last intake of gluten. So, one important takeaway is that gluten consumption or avoidance does not change the immune response to hepatitis B vaccine in patients with celiac disease. Over time, levels of antibody decreased in both groups, so doctors assessing immune response to hepatitis B vaccine should factor in the amount of time elapsed since vaccination, says Dr. Pérez. The prospective study involved 72 children with celiac disease who were vaccinated in the first year of life and whose antibody levels were below 10 mUI/mL. The researchers found no change in levels after the children received a single vaccine booster. In light of these results, the research team advises that children with celiac disease and undetectable levels of antibody be revaccinated with a full series of the vaccine. Source: 33rd Annual Meeting of the European Society for Paediatric Infectious Diseases (ESPID): Abstracts 463 and 464 and poster MPW06. Presented May 15, 2015.
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Celiac.com 05/18/2015 - It is well known that fermenting wheat flour with sourdough lactobacilli and fungal proteases reduces the amount of gluten. A team of researchers recently assessed whether patients with celiac disease can safely consume baked goods made from this hydrolyzed kind of wheat flour. The research team included Luigi Greco, Marco Gobbetti, Renata Auricchio, Raffaella Di Mase, Francesca Landolfo, Francesco Papro, Raffaella Di Cagno, Maria De Angelis, Carlo Giusseppi Rizzello, Angela Cassone, Gaetano Terrone, Laura Timpone, Martina D’Aniello, Maria Maglio, Riccardo Troncone, and Salvatore Auricchio. They are variously affiliated with the Department of Pediatrics and European Laboratory for the Study of Food Induced Diseases at the University of Naples, Federico II in Naples, and with the Department of Plant Protection and Applied Microbiology at the University of Bari in Bari, Italy. For their study, the team randomly assigned patients to receive 200 grams per day of natural flour baked goods (NFBG) (80,127 ppm gluten; n 6), extensively hydrolyzed flour baked goods (S1BG) (2480 ppm residual gluten; n 2), or fully hydrolyzed baked goods (S2BG) (8 ppm residual gluten; n 5) for 60 days. Two of the 6 patients who consumed natural flour baked goods discontinued the challenge due to adverse symptoms; all patients showed increased levels of anti–tissue transglutaminase (tTG) antibodies and mucosal damage to the small bowel. The 2 patients who ate the S1BG goods had no complaints and showed no symptoms, but developed subtotal atrophy. The 5 patients who ate the S2BG had no clinical symptoms or complaints. They showed no increase in anti-tTG antibodies, and their Marsh grades indicated no damage to small intestinal mucosa. The results showed that a 60-day diet of baked goods made from hydrolyzed wheat flour, manufactured with sourdough lactobacilli and fungal proteases, was not toxic to patients with celiac disease. Obviously further study is needed, along with a combined analysis of serologic, morphometric, and immunohistochemical parameters, which is the most accurate way to assess new celiac therapies. However, hydrolyzing wheat flour and treating it with sourdough lactobacilli and fungal proteases is not especially complicated. If these results stand, researchers may have developed the first wheat products that are safe for people with celiac disease. What do you think? Exciting news? Or one more thing to be skeptical about? Share your comments below. Source: CLINICAL GASTROENTEROLOGY AND HEPATOLOGY 2011;9:24 –29
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Celiac.com 03/24/2014 - Two new studies have confirmed colonization of gluten-degrading bacteria in the human mouth and in the upper gastrointestinal tracts respectively. Both studies come out of the Department of Periodontology and Oral Biology, Boston University Henry M. Goldman School of Dental Medicine in Boston, Massachusetts. The research teams included Maram Zamakhchari, Guoxian Wei, Floyd Dewhirst, Jaeseop Lee, Detlef Schuppan, Frank G. Oppenheim, and Eva J. Helmerhorst. Gluten is notoriously hard for mammals to digest, because gliadin proteins resist mammalian proteolytic enzymes in the gut, so researchers wanted to find sources of gluten-digesting microbial enzymes from the upper gastro-intestinal tract. These microbial enzymes have the potential to neutralize the gluten peptides that act as celiac disease triggers. In the first study the researchers assessed proteolytic activity in suspended dental plaque towards a) gliadin-derived paranitroanilide(pNA)-linked synthetic enzyme substrates a mixture of natural gliadins and c) synthetic highly immunogenic gliadin peptides (33-mer of α2-gliadin and 26-mer of γ-gliadin). In addition, they conducted gliadin zymography to establish the approximate molecular weights and pH activity profiles of the gliadin-degrading oral enzymes and performed liquid iso-electric focusing to determine overall enzyme iso-electric points. Their results provide the first known evidence of gluten-degrading microorganisms associated with the upper gastro-intestinal tract. Such microorganisms may play a hitherto unappreciated role in the digestion of dietary gluten and thus protection from celiac disease in subjects at risk. In the second study, the team employed a selective plating strategy using gluten agar to obtain oral microorganisms with gluten-degrading capacity. They then used16S rDNA gene sequencing to carry out microbial speciations. To determine enzyme activity, they used gliadin-derived enzymatic substrates, gliadins in solution, gliadin zymography, and 33-mer a-gliadin and 26-mer c-gliadin immunogenic peptides. They separated fragments of the gliadin peptides by RP-HPLC, and structurally characterized them using mass spectrometry. They found that strains Rothia mucilaginosa and Rothia aeria showed high gluten-degrading activity. For example, gliadins (250 mg/ml) added to Rothia cell suspensions (OD620 1.2) degraded by 50% after 30 minutes of incubation. Importantly, the 33-mer and 26-mer immunogenic peptides were also cleaved, primarily C-terminal to Xaa-Pro-Gln (XPQ) and Xaa-Pro-Tyr (XPY). The major gliadin-degrading enzymes produced by the Rothia strains were 70–75 kDa in size, and the enzyme expressed by Rothia aeria was active over a wide pH range (pH 3–10). While the human digestive enzyme system lacks the capacity to cleave immunogenic gluten, such activities are naturally present in the oral microbial enzyme repertoire. Taken together, these studies suggest a potential for these bacteria to fuel the development of compounds that can degrade of harmful gluten peptides that trigger celiac disease in susceptible individuals. Source: PLoS One. 2011;6(9):e24455. doi: 10.1371/journal.pone.0024455. http://www.ncbi.nlm.nih.gov/pubmed/20948997
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Celiac.com 08/28/2013 - Researchers at Washington State University are 'very close' to developing celiac-safe wheat strains, says lead project researcher Diter von Wettstein. Rich Koenig, associate dean and director of WSU Extension, says the wheat project involves removing the gluten material that causes the adverse reaction in people who have celiac disease. Von Wettstein says that his team has developed wheat hybrids that have 76.4 percent less gluten proteins than conventional strains, and that the next step is to eliminate the remaining percentage. Von Wettstein is working two distinct angles on this project. The first approach uses genetic modification, while the seconds does not. He acknowledges that doing it without genetic modification "would be better…But in the end, if the only way to do this is through genetic modification of wheat, it could still be a major advancement for people who suffer from that disease." The projects may still take a while as von Wettstein works to identify, selectively silence and remove the responsible genes. One caveat is that even if the project is successful, the wheat may not produce flour suitable for baking, though Koenig says that producing wheat suitable for people with celiac disease would be, nonetheless, an "important subsection of wheat production" Funding for von Wettstein's research is coming from The National Institutes of Health and Washington State's Life Science Discovery Fund.
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Celiac.com 07/03/2013 - Researchers have completed a genetic study of six autoimmune diseases, including diabetes, the largest such study of human disease genetics to date. The study will help scientists in their efforts to uncover the causes of these diseases, which include autoimmune thyroid disease, celiac disease, Crohn’s disease, psoriasis, multiple sclerosis and type 1 diabetes. While currently unknown, the underlying causes of these conditions are believed to involve a complex combination of genetic and environmental factors. In each of the six diseases, the identified genetic variants explained only a proportion of the heritability. Under one of the current major genetic disease hypotheses, the so called ‘rare-variant synthetic genome-wide association hypothesis,’ a small number of rare variants in risk genes are likely the major cause of the heritability of these conditions. In their study, the research team used high-throughput sequencing techniques, in an effort to identify new genetic variants, including rare and potentially high risk variants, in 25 previously identified risk genes taken from a sample of nearly 42,000 patients. Their data suggest that the genetic risk of these diseases more likely results from a complex interaction of hundreds of variants, each small on its own, but which, taken together impact the development of these six diseases. They estimate that rare variants in these risk genes make up only about three per cent of the heritability of these conditions that can be explained by common variants. The results, says lead study author David van Heel, suggest that "risk for these autoimmune diseases is not due to a few high-risk genetic variations." Rather, risk is likely due to a "random selection from many common genetic variants which each have a weak effect.” This could mean that it will never be possible to accurately predict a person's risk of developing any of these six autoimmune diseases, simply because there are too many variables. “However, the results do provide important information about the biological basis of these conditions and the pathways involved, which could lead to the identification new drug targets,” said van Heel. Source: Nature Genetics 42, 295–302 (2010). doi:10.1038/ng.543; and Firstpost.com.
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Can Bacteria Help Researchers Better Diagnose Celiac Disease?
Jefferson Adams posted an article in Latest Research
Celiac.com 01/30/2013 - Currently, doctors diagnose celiac disease with blood tests that screen for two antibodies, one that targets gluten and another that goes after an intestinal protein. The tests work pretty well to spot advanced cases of celiac disease, but by that time, patients are already suffering intestinal damage. A research team looking into a method for reliable earlier detection of celiac disease focused on the responses of certain bacteria to celiac disease. They have built a library of peptides on the surfaces of bacteria which capture new antibodies associated with celiac disease. This, in turn, has led them to a new technique for harvesting celiac disease antibodies, which may help improve diagnosis for celiac disease, especially early on. The researchers say the technique may allow them to successfully tell, much earlier than before, which perspective celiac sufferers are sick and which are healthy. The research team included Bradley N. Spatola, Joseph A. Murray, Martin Kagnoff, Katri Kaukinen, and Patrick S. Daugherty. They are affiliated with the Department of Chemical Engineering at the University of California at Santa Barbara, California, the Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota, the Laboratory of Mucosal Immunology, Department of Medicine and the Department of Pediatrics at the University of California at San Diego in La Jolla, California and with the Department of Gastroenterology and Alimentary Tract Surgery, Tampere University Hospital, Tampere, Finland. For their study, Patrick Daugherty, of the University of California, Santa Barbara, and his team aimed to find previously unknown disease-linked antibodies. Their strategy centered on building an enormous library of random peptide sequences to find ones that would bind to the antibodies. To create their library, the researchers inserted one billion random peptide genes into Escherichia coli, with one peptide gene per bacterium. Once the genes were expressed inside the bacteria, thousands of copies of the peptides migrated to the cells’ surface. The researchers hoped that some of these peptides would bind antibodies from the blood of people with early-stage celiac disease, but not those in samples from healthy people. The team hoped that their approach, with numerous bacteria each bearing a different peptide, would be more likely to identify unknown antibodies than are current types of peptide libraries, which must be mounted on hard surfaces. To test their new library approach, the researchers collected blood samples from 40 healthy people and 45 people who had been diagnosed with celiac disease. They purified antibodies from the blood samples, then labeled antibodies from half the celiac patients with a green fluorescent dye and the rest of the patients’ antibodies with a red dye. They then mixed the peptide-coated bacteria together with all the antibodies, adding five times as many unlabeled antibodies from the healthy subjects to block labeled antibodies from binding to peptides found in people with and without celiac disease. Next, they sorted the cells, collecting only those bacteria displaying both red and green fluorescence. Cells labeled with both dyes, the researchers reasoned, help a peptide that could bind to an antibody found in at least two people, one patient from each group. These antibodies, they say, could be markers for celiac disease. Additional screening of the peptides with antibodies from healthy patients and those with celiac disease, the researchers narrowed the bacterial pool down to six unique peptides, none of which bind to known celiac antibodies. The researchers then measured binding between these peptides and the full suite of antibodies from patients’ blood. Based on that data, they used a statistical analysis to conclude that they could identify correctly 85% of people with celiac disease and 91% of healthy – nearly matching the values of existing diagnostic tests. It remains uncertain whether this approach will permit doctors to diagnose celiac disease at earlier stages than current methods, but the results look promising, and the team remains hopeful. Daugherty says that the method is applicable to other immune disorders, including difficult-to-diagnose illnesses such as lupus, multiple sclerosis, and some cancers. Source: Anal. Chem., 2013, 85 (2), pp 1215–1222. DOI: 10.1021/ac303201d -
Lancet 2000;356:399-400. (Celiac.com 08/13/2000) According to a recent study by Dr. Antonio Gasbarrini and colleagues from Gemelli Hospital, Catholic University, in Rome, celiac disease may play a role in recurrent spontaneous abortion and intrauterine fetal growth retardation. The researchers studied 44 patients who had a history of spontaneous abortion, 39 patients who had fetuses with intrauterine growth retardation and 50 normal controls. For each group the researchers measured serum concentrations of IgA anti-endomysial and IgG anti-transglutaminase. According to Dr. Antonio Gasbarrini: The patients with recurrent spontaneous abortion and those with intrauterine fetal growth retardation had a significantly higher frequency of serological markers of celiac disease than controls, as reported in the July 29th issue of The Lancet. Further, they found that three patients with recurrent spontaneous abortion (8%) and six patients whose fetuses had growth retardation (15%) tested positive for celiac disease. In addition, nine of the patients also underwent an endoscopy (jejunal biopsy), and eight were positive for celiac disease. Of the positive endoscopy group three patients showed duodenal mucosa with chronic inflammation and subtotal villous atrophy and five patients presented with severe mucosal atrophy. The researchers also point out that while about 1 in 1000 people in Europe have some symptomatic gluten-sensitivity, it is now becoming clear that a greater proportion of individuals have a clinically silent form of the disease, and probably many others have a minor form of enteropathy. Their research shows that it is important to recognize celiac disease as a possible risk factor for recurrent spontaneous abortion and intrauterine fetal growth retardation, but it remains to be seen whether the removal of gluten from the diet will decrease the incidence of both problems for women with celiac disease.
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Celiac.com 10/03/2012 - In an effort to expand the market for Kansas-grown sorghum, a professor at Kansas State University and a group of food science graduate students are conducting research into the use of sorghum in new gluten-free food products for people with celiac disease. Kansas is one of the top sorghum producers in the U.S. In 2006, as the manufacturing of gluten-free products started to take off, sorghum farmers began looking for alternative uses for their crop. Fadi Aramouni, K-State professor of food science, said that quest triggered the university's research into sorghum as a gluten alternative. In America, sorghum has traditionally been used for animal feed, but the growing market for gluten-free foods, along with the availability of food-grade sorghum, is fueling the use of sorghum in these types of food products, he said. Aramouni said the research initially focused on developing a sorghum-based tortilla. He and the students looked at the six varieties of sorghum grown in Kansas and determined which one they thought would work best. They considered factors such as grain hardness, protein, carbohydrate and fiber content, shelf life, dough quality, and flavor. Right away, the research team ran into problems with milling, "because it turns out that the particle size during the milling will affect the properties of the sorghum flour," Armuni said. One problem is that sorghum tends to form a batter rather than a dough, so it is necessary to add eggs and other stabilizers, such as gums, to craft a suitable dough. Using the facilities at Kansas State's grain and science industry department, along with the U.S. Department of Agriculture laboratory in Manhattan, the research team has been able to create tortillas, breads, Belgian waffles and waffle cones from sorghum. Their research is largely funded by the Kansas Department of Agriculture, and includes comparing the glycemic index of their sorghum products to those made of wheat, corn and rice. The glycemic index measures how a given carbohydrate raises blood glucose. In the last few years, the team's sorghum-based creations have won first prize in the American Association of Cereal Chemists competition. using their new knowledge of sorghum, the researchers are now working to create gluten-free soft pretzels, sweet rolls and dinner rolls, vanilla-flavored Waffle Cones and Crunchums, a raspberry-jalapeno-flavored sorghum snack. "This is not cooking. This is science," Aramouni said. It is important science, he adds, because people who must eat gluten-free food need better, more nutritious products. What new gluten-free products would you like to see on the market? Share your comments below. Source: CJOnline.com
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Celiac.com 09/21/2012 - Refractory celiac disease type II (RCDII) is a severe complication of celiac disease that occurs when symptoms and intestinal damage continue even when the patient adopt a gluten-free diet. Refractory celiac disease marked by abnormal intraepithelial lymphocytes (IELs) of unknown origin that display an atypical CD3(-)CD7(+)icCD3(+) phenotype. About 40% of patients with RCDII lymphocytes develop a dangerous and invasive lymphoma. A team of researchers recently sought to identify possible origins of abnormal intraepithelial lymphocytes in refractory celiac disease type II. The research team included F. Schmitz; T.M. Tjon, Y. Lai; A. Thompson; Y. Kooy-Winkelaar; R.J. Lemmers; H.W. Verspaget; M.L. Mearin; F.J. Staal; M.W. Schreurs; T. Cupedo; A.W. Langerak; C.J. Mulder; J. van Bergen; and F. Koning. In their study, the researches sought to find the physiological counterpart of these abnormal intraepithelial lymphocytes cells. To do so, they used microarray analysis, real-time quantitative PCR and flow cytometry to compare RCDII cell lines with T-cell receptor positive (TCR(+)) IEL (T-IEL) lines. They then used their data to identify cells with an RCDII-associated phenotype in duodenal biopsies from non-refractory individuals by multicolor flow cytometry. They found that RCDII cell lines were distinct from T-IEL lines and showed higher levels of multiple natural killer (NK) cell receptors. In addition to the CD3(-)CD7(+)icCD3(+) phenotype, the RCDII lines showed an absence of CD56, CD127 and CD34, compared with other lymphocyte subsets. Moreover, they found cells matching this surface lineage-negative (Lin(-)) CD7(+)CD127(-)CD34(-) phenotype that showed a functional interleukin-15 (IL-15) receptor and comprised a substantial portion of IELs in duodenal specimens of patients without celiac disease, particularly children. They also found cells of this kind in the thymus. For patients without celiac disease, the Lin(-)CD7(+)CD127(-)CD34(-) subset was one of four subsets within the CD3(-)CD7(+)icCD3(+) population that showed a differential expression of CD56 and/or CD127. The results indicate that the CD3(-)CD7(+)icCD3(+) population is heterogeneous and show the existence of a Lin(-) subset that is different from T, B, NK and lymphoid tissue inducer cells. The team hypothesizes that the IL-15 cells are the counterpart of abnormal cells that are expanded in RCDII and transformed in RCDII-associated lymphoma. Source: Gut. 2012 Jul 6.
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Celiac.com 09/06/2012 - Researchers at the Department of Food Technology of the Universidad Politécnica de Madrid have used teff flour to develop a new biscuit they claim is suitable for "celiac patients and sportsmen." Teff (Eragrostis tef) is an annual grass, a species of lovegrass, native to the northern Ethiopian and Eritrean highlands of Northeast Africa. Flour made from teff grains has been used in local bread products for centuries. Before you picture a light, fluffy, fresh-from-the-oven biscuit, it's important to remember that the Europeans use the term biscuit for what Americans call a 'cracker.' So, the final product is likely something drier and crunchier than the American biscuit, and much more like an American cracker. The developers have applied for a patent on their process, and say that manufacturers will be able to use the process to create new products once it is granted. One of the current challenges for manufacturers of gluten-free foods is to modify their production process in order to mimic the natural, chewy, elastic properties that are inherent to wheat flour. That challenge is one reason so many gluten-free products are dry and brittle. That is not true of this new product, say the researchers. Unlike many non-wheat flours, teff has a "high capacity to absorb water and act also as binder in the dough, alleviating the problems deriving from the absence of gluten in cereal,” said the researchers. According to the research team, 100g of teff contains between 9 and 15 grams of protein, 73 grams of carbohydrates, 2 grams of fat and 3 grams of fiber. This means that their product needs no added fats or artificial thickeners commonly used in other gluten-free foods, which reduces calories and improves texture and flavor. Moreover, the biscuits can be made using existing manufacturing processes. Teff also has a remarkable essential amino acids profile, note the researchers. It is high in zinc and iron, and has a naturally low glycemic index, resulting in a slow breakdown of its carbohydrates. The resulting product, they say, will appeal to athletes, diabetics and people with anemia, and celiac disease, and will likely sell at a lower price than similar products. Other than teff flour, the biscuits also include skimmed milk, nonfat plain yogurt, brown sugar, defatted cocoa powder, orange zest and hazelnuts. Source: Nutraingredients.com
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Celiac.com 06/08/2012 - In a new study, researchers at Brigham and Women's Hospital (BWH) addressed whether the genetic risk of the most common medical conditions, including celiac disease, stems from many rare mutations that each confer a high degree of risk in various people, or from common differences throughout the genome that modestly influence risk. They used data and new analysis tools to assess new methods to better understand gene mutations for celiac and three other diseases, rheumatoid arthritis, coronary artery disease and myocardial infarction (heart attack); and type 2 diabetes. The researchers developed a new statistical method that used what is called "polygenic risk score analysis," to estimate the heritable genetic markers of these diseases that is explained by common differences across the genome. The method makes use of data from earlier genome-wide association studies, or GWAS, an approach used to scan DNA samples for common genetic markers seen throughout the population—called SNPs (single nucleotide polymorphisms). For rheumatoid arthritis, the team used computer simulations to show that the underlying genetic risk is largely due to many common alleles rather than rare mutations. They observed similar results for celiac disease (43 percent), myocardial infarction (48 percent) and type 2 diabetes (49 percent). "What is remarkable," says senior author Robert Plenge, MD, PhD, BWH director of Genetics and Genomics in the Division of Rheumatology, Immunology and Allergy, "is that our statistical model was broadly applicable to several common diseases, not just rheumatoid arthritis...Our study provides a clear strategy for discovering additional risk alleles for these and likely many other common diseases." According to the researchers, these methods can be applied to other genome-wide datasets (e.g., GWAS or whole genome sequencing) to estimate the degree to which there is a genetic component. Source: Nature Genetics 44, 483–489 (2012) doi:10.1038/ng.2232
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