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  • Jefferson Adams
    Jefferson Adams

    Peptide in Durum Wheat May Protect Against Effects of Celiac Disease

    Celiac.com 05/08/2007 - One of the strategies for developing alternative therapies for treating celiac disease centers on the identification of antagonist peptides that might inhibit the abnormal immune response caused by gliadin peptides in celiac disease.

    A recent study published in the journal Pediatric Research indicates that a peptide that occurs naturally in durum wheat may protect against the effects of celiac disease by acting as an antagonist against gliadin peptides associated with abnormal immune response.

    The study was conducted by a team of Italian researchers made up of Drs. Marco Silano, Rita DiBenedetto, Antonello Trecca, Gioachhino Arrabiato, Fabiana Leonardi, Massimo De Vincenzi.

    The research team set out to assess the antagonistic effects of 10mer, a decapeptide (sequence QQPQDAVQPF) from the alcohol–soluble protein portion of durum wheat, and to evaluate its prospects for preventing gliadin peptides from activating celiac peripheral blood lymphocytes.

    The team extracted peripheral blood mononuclear cells from children with celiac disease who tested DQ2-positive, and from a healthy control group. These samples were then incubated with the peptic-tryptic digest of bread wheat gliadin (GLP) and peptide 62-75 from [alpha]-gliadin, both alone and separately with 10mer.

    PBMC proliferation, release of pro-inflammatory Th1 cytokines interferon-[gamma] and tumor necrosis factor-[alpha], release of immuno-regulatory cytokine IL-10, and analysis of CD25 expression as indexes of lymphocytes activation were performed.

    Exposure to wheat gliadin peptide and peptide 62-75 from [alpha] gliadin both showed increased activation of lymphocytes. However, the incubation samples with 10mer showed inhibited lymphocyte action.

    The study indicates that naturally occurring peptide 10mer in durum wheat may protect against lymphocyte activity in patients with celiac disease, and that further study and evaluation of these findings is warranted.

    Pediatric Research. 61(1):67-71, January 2007.


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    I didn't understand the medical terms in this article, but I did get an understanding out of the rest I think. Sorry but I don't know much about medical terms but I will learn.

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  • About Me

    Jefferson Adams earned his B.A. and M.F.A. at Arizona State University, and has authored more than 2,000 articles on celiac disease. His coursework includes studies in biology, anatomy, medicine, science, and advanced research, and scientific methods. He previously served as Health News Examiner for Examiner.com, and devised health and medical content for Sharecare.com. Jefferson has spoken about celiac disease to the media, including an appearance on the KQED radio show Forum, and is the editor of the book "Cereal Killers" by Scott Adams and Ron Hoggan, Ed.D.

  • Related Articles

    Scott Adams
    Arch Dis Child 2006;91:39-43.
    Celiac.com 12/08/2005 – Researchers in the United Kingdom conducted a systematic review and meta-analysis of 15 studies published between 1966 and 2004 that evaluated the association between breast-feeding and celiac disease. Their review covered more than 4,000 children and found that breast-feeding may offer protection against the development of celiac disease, especially if it is prolonged and covers the period when gluten is introduced. It was unclear, however, whether breast-feeding merely delays the onset of symptoms, or actually offers permanent protection against the disease, and more long-term prospective cohort studies will be necessary to make such a determination.

    Roy Jamron
    Celiac.com 02/10/2008 - Researchers have found a 10mer durum wheat peptide capable of shifting a Th1 gluten-intolerant T cell response to a Th2 gluten-tolerant T cell response in intestinal T cell cultures derived from celiac disease children and incubated with deamidated gliadin peptides.  Durum wheat peptides could potentially treat celiac disease by causing celiac disease associated T cells to react tolerantly to gluten.
    In the study, incubation of the T cell cultures with deamidated gliadin peptides resulted in a significant increase in T cell proliferation and interferon-gamma release.  Simultaneous exposure to duram wheat peptides totally abolished the cell proliferation and cytokine release while maintaining an elevated release of interleukin-10 (IL-10).
    The workings of the immune system are too complex to discuss here in detail.  Basically when a "pre-helper" CD4-type T cell is presented with an epitope from an antigen (gliadin), the T cell becomes activated and responds to the stimulus by becoming either a type 1 or type 2 helper T cell which in turn releases different subsets of cytokines.  The Th1 path promotes mucosal tissue destruction in celiac disease while the Th2 path initiates proliferation of gluten and tTGase antibodies.  Th1 and Th2 cytokines each have properties which act in a feedback loop to suppress, limit, and regulate each other's cytokine secretions, i.e. Th1 cytokines suppress Th2 cytokine secretion and vice vesa.
    Overactivity of either a Th1 or a Th2 response can result in an autoimmune condition.  Researchers theorize that balancing Th1/Th2 response can ameliorate and control symptoms and disease progression in at least some autoimmune diseases.  Th1 response includes release of the cytokine interferon-gamma which differentiates and activates macrophages.  Th2 response can include the release of IL-10, a cytokine which suppresses inflammation and promotes antigen tolerance.  Various molecules have been demonstrated to shift Th1/Th2 response in various autoimmune disorders.  In the durum wheat study, the presence of the durum wheat peptide in the gliadin peptide incubated celiac intestinal T cell culture increased Th2 IL-10 release and stopped T cell proliferation and Th1 interferon-gamma release.  Hence, this durum wheat peptide may be useful as a celiac disease therapy.  How effective this treatment may be is unknown at this time. 
    Below is an example of sodium benzoate being used to shift Th1 to Th2 response in a mouse model of multiple sclerosis which improved symptoms and disease progression when fed to the mice orally.  This suggests that the durum wheat peptide could potentially treat celiac disease by simply being administered as an oral supplement.  However, if a probiotic bacteria could be genetically engineered to continuously secrete a form of this durum wheat peptide in the gut, this could result in essentially a "cure" for celiac disease if the durum wheat peptide proves effective.
    ----------
    Am J Clin Nutr. 2008 Feb;87(2):415-23.
    A 10-residue peptide from durum wheat promotes a shift from a Th1-type response toward a Th2-type response in celiac disease.
    Silano M, Di Benedetto R, Maialetti F, De Vincenzi A, Calcaterra R, Trecca A, De Vincenzi M.
    Division of Food Science, Human Nutrition and Health, Istituto Superiore di Sanita, Rome, Italy.
    http://www.ajcn.org/cgi/content/abstract/87/2/415
    ----------
    J Immunol. 2007 Jul 1;179(1):275-83.
    Sodium benzoate, a food additive and a metabolite of cinnamon, modifies T cells at multiple steps and inhibits adoptive transfer of experimental allergic encephalomyelitis.
    Brahmachari S, Pahan K.
    Department of Neurological Sciences, Rush University Medical Center, 1735 West Harrison Street, Chicago, IL 60612, USA.
    http://www.jimmunol.org/cgi/content/abstract/179/1/275
    * * *

    Jefferson Adams
    Celiac.com 04/07/2008 - No, this is not some kind of April Fool’s joke.When I read this report, I just about fell off my chair. New research indicates thatbeing poor and living in squalor might actually provide some benefitagainst the development of celiac disease.
    A team of medicalresearchers recently set out to examine gene-environmental interactionsin the pathogenesis of celiac disease. The research team was made up ofA. Kondrashova, K. Mustalahti, K. Kaukinen, H. Viskari, V. Volodicheva,A. M. Haapala, J. Ilonen, M. Knip, M. Mäki, H. Hyöty, T. E. Group.Finland and nearby Russian Karelia have populations that eat about thesame amounts of the same grains and grain products. The two populationsalso have a high degree of shared genetic ancestry. The only majordifference between the populations of the two areas lies in theirsocioeconomic conditions.
    The region of Russian Karelia ismuch poorer than the neighboring areas in nearby Finland. Thesanitation levels in Russian Karelia are also distinctly inferior thanthey are in Finland. The researchers compared the prevalence of celiacdisease and predisposing human leukocyte antigen (HLA) alleles inpopulations from Russian Karelia and Finland. The team performedscreening for tissue transglutaminase antibodies (tTG) and HLA-DQalleles on 1988 school-age children from Karelia and 3654 children fromFinland. Children with transglutaminase antibodies were encouraged tohave a duodenal biopsy.
    Interestingly, the patients fromRussian Karelia showed tTG antibodies far less often than their Finnishcounterparts (0.6% compared to 1.4%, P = 0.005). The patients fromRussian Karelia also showed Immunoglobulin class G (IgG) antigliadinantibodies far less frequently than their Finnish patients (10.2%compared to 28.3%, P<0.0001).
    The researchers confirmed adiagnosis of celiac disease by duodenal biopsy in four of the eighttransglutaminase antibody-positive Karelian children, for an occurrencerate of 1 in 496 versus 1 in 107 Finnish children.
    In bothgroups, the same HLA-DQ alleles were associated with celiac disease andthe presence of transglutaminase antibodies. The patients from RussianKarelia showed a much lower prevalence of transglutaminase antibodiesand celiac disease than the Finnish children. 
    The poorconditions and inferior hygienic conditions in Russian Karelia mightprovide some kind of protection against the development of celiacdisease. The value of studies like this aren’t to make us wax nostalgicfor poverty, or to encourage people to fend off celiac disease bybecoming poor and living in squalid conditions. The value of a studylike this lies in the idea that there may be more to the development ofceliac disease than simple biological factors. That environmentalconditions might play a key role in both the frequency ofceliac-related antibodies, and in the development of the disease itselfis quite intriguing and clearly warrants further and more comprehensivestudy.
    Ann Med. 2008;40(3):223-31.


    Jefferson Adams
    Celiac.com 02/03/2010 - Celiac disease increases production of IL-17A by cells that also make IFN-gamma. Recently, a research team set out to characterize the expression of IL-17A-producing cells in celiac disease.
    The team included I. Monteleone, M. Sarra, G. Del Vecchio Blanco, O. A. Paoluzi, E. Franzè, D. Fina, A. Fabrizi, T. T. Macdonald, F. Pallone, and G. Monteleone of the Department of Internal Medicine at the University of Tor Vergata in Rome, Italy.
    Infiltration of the mucosa with IFN-gamma-secreting Th1 cells is one of the features associated with celiac disease. Recent studies have shown the pathogenic effects previously attributed to Th1 cells may in fact be caused by a novel subset of T cells, termed Th17 cells, and noted for expressing high levels of IL-17A.
    In this study, the team set out to characterize the expression of IL-17A-producing cells in celiac disease. Using real-time PCR and ELISA, the team showed that expression of IL-17A RNA and protein is greater in active celiac disease biopsy specimens than in specimens from inactive celiac disease, and normal mucosal biopsies.
    Through flow cytometry, the team confirmed that the mucosa of celiac disease patients overproduces IL-17A, and that the main sources for this overproduction were CD4(+) and CD4(+)CD8(+) cells.  Most IL-17A-producing CD4(+) and CD4(+)CD8(+) cells co-expressed IFN-gamma but did not co-express CD161.
    Including a peptic-tryptic digest of gliadin to ex-vivo organ cultures of duodenal biopsy specimens taken from patients with inactive celiac disease enhanced IL-17A production 
    by both CD4(+) and CD4(+)CD8(+) cells.
    Since the team showed earlier that patients with celiac disease overproduced IL-21, a T cell-derived cytokine involved in the control of Th17 cell responses, they next determined whether IL-21 was responsible for regulating IL-17A expression.
    Blocking IL-21 action with a neutralizing IL-21 Ab lowered total IL-17A expression in cultures of active celiac disease and peptic-tryptic digest of gliadin-treated celiac disease biopsy specimens.
    From the data, the team concludes that celiac disease increases IL-17A, which is produced by cells that also produce IFN-gamma.
    Source: Journal of Immunology, 2010 Jan 8.


    Destiny Stone
    The Cesarean Section and Celiac Disease Connection
    Celiac.com 05/20/2010 - In Germany, a team of scientists led by Doctor Mathias Hornef of Hannover Medical School, acknowledged that people with inflammatory diseases like celiac, Crohn's and ulcerative colitis, have a different chemical mix of bacteria in their intestines. They also knew that the method in which  a child is delivered can affect their bacteria mixture. It was this information that led the team of scientists to speculate if  children with celiac, Crohn's or ulcerative colitis had a higher incident of cesarean births.
    Doctor Hornef and his colleagues studied children and adolescents with celiac, Crohn's and ulcerative colitis, as well as children with other gastrointestinal complications. They also studied a control group of children with unrelated conditions.
    The results clearly demonstrated that the children with the highest rate was the celiac group with 28% of them born by cesarean section. The other four groups had no more than 19% born by cesarean section. Coincidentally, the average celiac child was diagnosed earlier than the other patients used for this study.
    Doctor  Hornef's findings  were a scientific breakthrough previously undocumented by any other scientist. No link has ever been established between children with celiac disease and cesarean deliveries. The results of the study have led to much speculation in the scientific community as to why the celiac children had a higher rate of cesarean births compared to the children with the Crohn's and ulcerative colitis, being that they are  all inflammatory diseases which develop in many related ways.
    Hornef said one explanation of the celiac C-section connection  could be that celiac disease is often stimulated  early  in life and therefore, those newborns born with abnormal intestinal bacteria may be especially susceptible to C-section births.
    Other scientists unrelated to this study were very interested in the results, but didn't exclude the other possibilities that may not involve the method of birth for the babies.
     Director of clinical research  at the Celiac Disease Center at Boston's Beth Isreal Deaconess Medical Center, Doctor Leffler, suggested that since celiac is a genetic disease, many of the children with celiac may have had mother's with undiagnosed celiac. Undiagnosed celiac disease can cause complications in the birthing process and would explain the increased number of cesarean section births among that population. Dr. Leffler sites the growing awareness of celiac disease as a possibility for more diagnosed children than mothers. He stated  that the study results may actually be an indication that doctors should be testing for celiac disease in young women looking to become pregnant. Doctor Leffler further stated that early celiac  diagnosis and a gluten-free diet decreases the chances of a cesarean birth, and renders mothers just as likely to be at risk for a cesarean section as the general public. Leffler added that untreated celiac disease can also effect the fetus by things like, a slower growth rate and an increased risk of premature births.
    Doctor Joseph Murray of the Rochester, Minnesota Mayo Clinic is a gastrointestinal doctor that specializes in celiac disease. Doctor Murray suggested initiating a study to evaluate the possible link between cesarean birth and diabetes, since diabetes is substantially related to celiac disease.
    Doctor Hornef adamantly emphasized that cesarean sections can be lifesaving for many babies. Furthermore, Doctor Hornef  does not advocate avoiding cesarean births. He said that  larger studies and more data is needed before any conclusions can be made with the connection between celiac disease and cesarean section births.
    Source:

    doi:10.1542/peds.2009-2260
     



    Gryphon Myers
    New Study Points to Antibiotics as Celiac Disease Risk Factor
    Celiac.com 07/22/2013 - Celiac disease is known to be caused by a combination of genetic and environmental factors. The genetic markers are fairly well established by now, but the environmental factors that are associated with celiac disease are still pretty foggy. A recent study suggests that antibiotic use might be one such factor.
    In a population-based case-control study analyzing Swedish population data, antibiotic use was compared against diagnosis of celiac disease. 2,933 people with celiac disease diagnoses were linked to the Swedish Prescribed Drug Register, in order to provide a history of antibiotic use. 2,118 people with inflammation (early celiac disease) and 620 people with normal mucosa but positive celiac disease blood test results were also compared. The control group consisted of 28,262 individuals matched for age and sex from the general population.
    The results of the study significantly suggest that antibiotic use is associated with celiac disease, at an odds ratio of 1.4 (1.27-1.53 confidence interval). Early celiac disease was also connected, with an odds ratio of 1.90 (1.72-2.10 confidence ratio), as well as positive celiac disease blood tests, at 1.58 odds ratio (1.30-1.92 confidence interval). Even when antibiotic use in the last year was ruled out, the results were very similar at 1.30 odds ratio (1.08-1.56 confidence interval). When ruling out patients with additional diseases, which could potentially be factors, the results were also very similar at 1.30 odds ratio (1.16-1.46 confidence interval).
    What does all that mean? A 1.4 odds ratio basically means that people who had a history of antibiotic use were 1.4 times as likely as those who had not taken antibiotics to develop celiac disease. The fact that inflammation associated with early celiac disease was also highly connected suggests that antibiotics' role in disrupting the biology of the GI tract could in some way cause celiac disease. There is still some question of causality, but it would seem that antibiotics could very likely be a culprit in the development of celiac disease, and should be avoided when possible.
    Source:
    http://www.biomedcentral.com/1471-230X/13/109/abstract

    Jefferson Adams
    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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    Im the same, I never know what to eat, some food does better than others for me, I went on to make my own soup and Im glad I did, I should do it more often and at least then J know what's going in to it, it wasn't the best first try but I enjoyed it haha
    Thank you for the advice, in the end I went and made my own soup, not great for my first try but it was better than potentially making myself worse, I enjoyed it, I got some vitamains too to take, I was able to find a liquid Vitamain B Complex, the store I went to was helpfull enough to show me what was Gluten Free.   I fealt awful around then, Im feeling like I have more energy now I can actually do things and focus more, Ill keep on like I have been, Im not 100% and still have some B
    Not to mention the fact that (for those using the Nima) the Nima sensor has been known to give false positives. https://www.theverge.com/2019/4/1/18080666/nima-sensor-testing-fda-food-allergy-gluten-peanut-transparency-data https://www.celiac.ca/cca-statement-nima-gluten-sensor/ https://www.allergy-insight.com/nima-is-it-really-96-9-accurate/ https://www.glutenfreewatchdog.org/news/troubling-gluten-testing-data-released-by-nima-but-hold-the-phone/ https://www.glutenfreew
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