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Celiac.com 03/02/2016 - A team of researchers recently completed the first extensive study comparing gene expression in children and adults with celiac disease, and found some key differences between the two groups. The research team included V. Pascual, L. M. Medrano , N. López-Palacios, A. Bodas, B. Dema, M. Fernández-Arquero, B. González-Pérez, I. Salazar, and C. Núñez. They are variously affiliated with Servicio de Pediatría, Servicio de Aparato Digestivo, and Servicio de Inmunología Clínica at the Instituto de Investigación Sanitaria del Hospital Clínico San Carlos (IdISSC), Madrid, Spain, and with the Departamento de Producción Animal, Facultad de Veterinaria, and the Departamento de Estadística e Investigación Operativa I, Facultad de Matemáticas, Universidad Complutense de Madrid in Madrid, Spain. For their study, the team collected 19 duodenal biopsies of children and adults with celiac disease and compared the expression of 38 selected genes between each other, and in 13 non-celiac disease control subjects matched by age. The team used a Baysian methodology to analyze the differences of gene expression between groups. They found that, compared to controls, children and adults with celiac disease all had seven genes with a similarly altered expression. These were C2orf74, CCR6, FASLG, JAK2, IL23A, TAGAP and UBE2L3. The team found differences in 13 genes, six of which were altered only in adults (IL1RL1, celiac disease28, STAT3, TMEM187, VAMP3 and ZFP36L1) and two only in children (TNFSF18 and ICOSLG); while four genes show a significantly higher alteration in adults (CCR4, IL6, IL18RAP and PLEK) and one in children (C1orf106). Between the two groups, the team found significant differences in the expression level of several genes, most notably the higher alteration seen in adults. The team is calling for further research to assess possible genetic influences behind the changes, along with the specific physical consequences of the reported differences. Source: PLOS.ORG. Published: February 9, 2016. DOI: 10.1371/journal.pone.0146276
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Celiac.com 03/30/2011 - A team of medical researchers set out to compare gut permeability and mucosal immune gene expression in celiac disease and gluten sensitivity. The research team included Anna Sapone, Karen M Lammers, Vincenzo Casolaro, Marcella Cammarota, Maria T Giuliano, Mario De Rosa, Rosita Stefanile, Giuseppe Mazzarella, Carlo Tolone, Maria I Russo, Pasquale Esposito, Franca Ferraraccio, Maria Carteni, Gabriele Riegler, Laura de Magistris and Alessio Fasano. People with celiac disease suffer an adverse autoimmune reaction when they consume gluten. People with gluten-sensitivity cannot tolerate gluten and may develop gastrointestinal symptoms similar to those in celiac disease. However, for people with gluten intolerance, the overall clinical picture is usually less severe, and is not accompanied by the concurrence of tissue transglutaminase autoantibodies or autoimmune comorbidities. By examining and comparing mucosal expression of genes associated with intestinal barrier function, along with innate and adaptive immunity the team sought to better understand the similarities and differences between celiac disease and gluten sensitivity. For their study, the team enrolled a group of subjects with celiac disease, a group with gluten sensitivity, and a control group of healthy, gluten-tolerant individuals. They assessed intestinal permeability using a lactulose and mannitol probe, and collected mucosal biopsy specimens to study the expression of genes involved in barrier function and immunity. They found that gluten sensitivity, unlike celiac disease, is not associated with increased intestinal permeability. In fact, subjects with gluten sensitivity showed significantly reduced intestinal permeability compared with controls (P = 0.0308). This was accompanied with significantly increased expression of claudin (CLDN) 4 (P = 0.0286). Relative to controls, subjects with celiac disease expressed higher levels of adaptive immunity markers interleukin (IL)-6 (P = 0.0124) and IL-21 (P = 0.0572), while those with gluten sensitivity showed no higher levels. Subjects with gluten intolerance showed increased expression of the innate immunity marker Toll-like receptor (TLR) 2, but subjects with celiac disease showed no such increase (P = 0.0295). Finally, subjects with gluten intolerance showed significantly reduced expression of the T-regulatory cell marker FOXP3 relative to controls (P = 0.0325) and celiac subjects (P = 0.0293). This study supports the existence of gluten sensitivity and celiac disease as two clinically different gluten-associated disorders. The study also supports the characterization of gluten sensitivity as a condition associated with prevalent gluten-induced activation of innate, rather than adaptive, immune responses in the absence of detectable changes in mucosal barrier function. Source: BMC Medicine 2011, 9:23 doi:10.1186/1741-7015-9-2
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Celiac.com 02/18/2015 - It's well documented that HLA-DQ molecules play a role in the pathogenesis of celiac disease through the presentation of gluten peptides to CD4(+) T cells. The α- or β-chain sharing HLA molecules DQ2.5, DQ2.2, and DQ7.5 display different risks for the disease. Researchers have recently showed that T cells of DQ2.5 and DQ2.2 patients recognize distinct sets of gluten epitopes, which indicates that these two DQ2 variants select different peptides for display. To figure out if this is the case, the research team performed a comprehensive comparison of the endogenous self-peptides bound to HLA-DQ molecules of B-lymphoblastoid cell lines. The research team included E. Bergseng, S. Dørum, M. Arntzen, M. Nielsen, S. Nygård, S. Buus, G.A. de Souza, and L.M. Sollid. They are variously affiliated with the Centre for Immune Regulation, Department of Immunology, University of Oslo and Oslo University Hospital-Rikshospitalet, Oslo, Norway. The team began by isolating peptides from affinity-purified HLA molecules of nine cell lines. They then subjected the isolated peptides to quadrupole orbitrap mass spectrometry and MaxQuant software analysis. They identified 12,712 endogenous peptides at very different relative abundances. Hierarchical clustering of normalized quantitative data revealed significant differences in repertoires of peptides between the three DQ variant molecules. They identified peptide-binding motifs using the neural network-based method, NNAlign. The binding motifs of DQ2.5 and DQ7.5 concurred with previously established binding motifs, but the binding motif of DQ2.2 was remarkably different from that of DQ2.5, with position, P3 being a major anchor having a preference for threonine and serine. This is interesting for the reason that three recently identified epitopes of gluten recognized by T cells of DQ2.2 celiac patients harbor serine at position P3. This study shows that relative quantitative comparison of endogenous peptides sampled from our protein metabolism by HLA molecules can provide clues to understand HLA association with disease. Source: Immunogenetics. 2015 Feb;67(2):73-84. doi: 10.1007/s00251-014-0819-9. Epub 2014 Dec 12.
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Celiac.com 07/24/2013 - Gastrointestinal symptoms are a common feature in children with autism, drawing attention to a potential association with celiac disease or gluten sensitivity. So far, studies of the immune response to gluten in autistic individuals, along with its association with celiac disease have produced inconsistent data. A team of researchers recently set out to assess immune reactivity to gluten in children diagnosed with autism according to strict criteria, and to evaluate the potential link between autism and celiac disease. The research team included Nga M. Lau, Peter H. R. Green, Annette K. Taylor, Dan Hellberg, Mary Ajamian, Caroline Z. Tan, Barry E. Kosofsky, Joseph J. Higgins, Anjali M. Rajadhyaksha, and Armin Alaedini. For their study, the team assessed 37 children (with or without gastrointestinal symptoms) diagnosed with autism according to both the Autism Diagnostic Observation Schedule (ADOS) and the Autism Diagnostic Interview, Revised (ADI-R), 27 unaffected siblings, and 76 age-matched healthy controls. They then tested blood specimens for antibodies to native gliadin, deamidated gliadin, and transglutaminase 2 (TG2). They then genotyped all children with positive antibody tests for celiac disease associated HLA-DQ2 and -DQ8 alleles. The team found that children with autism had substantially higher levels of IgG antibodies compared with unrelated healthy controls (p<0.01). The IgG levels were also higher compared to the unaffected siblings, but were not statistically significant. Autistic children with gastrointestinal symptoms showed significantly greater IgG anti-gliadin antibody response, compared to those without them (p<0.01). All groups showed similar IgA response to gliadin across groups. Both study subjects and control subjects ahd similar levels of celiac disease-specific serologic markers, i.e., antibodies to deamidated gliadin and TG2. The researchers found no association between increased anti-gliadin antibody and presence of HLA-DQ2 and/or -DQ8. Some children with autism do show a type of increased immune reactivity to gluten which appears to be different from celiac disease. The increased anti-gliadin antibody response and its association with GI symptoms suggests that these children may suffer from immunologic and/or intestinal permeability abnormalities. Source: PLOS Online
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Celiac.com 01/04/2013 - Currently, doctors must still use invasive techniques to distinguish between uncomplicated and complicated forms of celiac disease. In an effort to find a non-invasive approach to the issue, a research team recently set out to investigate the potential use of novel serum parameters, including IL-6, IL-8, IL-17, IL-22, sCD25, sCD27, granzyme-B, sMICA and sCTLA-4 in patients diagnosed with active celiac disease, celiac disease on a GFD, Refractory coeliac disease (RCD) type I and II, and enteropathy associated T-cell lymphoma (EATL). The research team included Greetje J. Tack, Roy L. van Wanrooij, B. Mary Von Blomberg, Hedayat Amini, Veerle M. Coupe, Petra Bonnet, Chris J. Mulder and Marco W. Schreurs. Their investigation revealed elevated levels of the pro-inflammatory IL-8, IL-17 and sCD25 in both active celiac disease and in refractory celiac disease, types I and II. They also found that RCDII patients displayed higher serum levels of soluble granzyme-B and IL-6 in comparison to active celiac disease patients. Furthermore, EATL patients showed higher levels of IL-6 as compared to all other groups. Otherwise, the team found no differences between RCDI and active celiac disease or RCDII. These novel serum parameters show distinct immunological differences in RCDII and EATL, compared with uncomplicated celiac disease and RCDI. Source: BMC Gastroenterology 2012, 12:159. doi:10.1186/1471-230X-12-159
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Celiac.com 12/03/2012 - Gluten sensitivity has recently been added to the spectrum of gluten-related disorders, but precise diagnostic markers do not yet exist. A research team recently set out to understand the blood test pattern of gluten sensitivity, and to compare it with the blood test pattern seen in celiac disease. The researchers included U. Volta, F. Tovoli, R. Cicola, C. Parisi, A. Fabbri, M. Piscaglia, E. Fiorini, G. Caio, of the Department of Clinical Medicine at University of Bologna's St. Orsola-Malpighi Hospital in Bologna, Italy. For their study, the researchers looked at blood samples from 78 patients with gluten-sensitivity and 80 patients with celiac disease. They assessed levels of immunoglobulin (Ig)G/IgA antigliadin antibodies (AGA), IgG deamidated gliadin peptide antibodies (DGP-AGA), IgA tissue transglutaminase antibodies (tTGA), and IgA endomysial antibodies (EmA). They found positive readings for IgG AGA in 56.4% of patients with gluten-sensitivity, and in 81.2% of patients with celiac disease. Antibody levels for both groups were in the high range. They found IgA AGA in 7.7% of patients with gluten-sensitivity, and in 75% of patients with celiac disease, which shows lower enzyme-linked immunosorbent assay activities in gluten-sensitivity patients than in patients with celiac disease. Only 1 of the 78 patients with gluten-sensitivity tested positive for IgG DGP-AGA, which was found in nearly 90% of patients with celiac disease. All patients with gluten-sensitivity tested negative for IgA tTGA and IgA EmA, while 98.7% of patients with celiac disease tested positive for IgA tTGA, and 95% were positive for IgA EmA. Patients with gluten-sensitivity presented a variety of intestinal and extra-intestinal symptoms, including abdominal pain, bloating, diarrhea, constipation, foggy mind, tiredness, eczema/skin rash, headache, joint/muscle pain, numbness of legs/arms, depression, and anemia. Small intestinal mucosa for these patients was either normal or only mildly abnormal. The data from these blood tests show that more than half of patients with gluten sensitivity will test positive for IgG AGA, and a small number will test positive for IgA AGA, but none will show positive results for EmA, tTGA, and DGP-AGA, which are the specific markers of celiac disease. Source: J Clin Gastroenterol. 2012 Sep;46(8):680-5.
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Celiac.com 11/29/2007 - Studies have documented the role of gut microbiotic bacteria in diseases involving chronic inflammation, such as celiac disease, yet there is scant data on such bacteria that is specific to people with celiac disease. A team of Spanish and Italian researchers from three different hospitals and universities made up of Yolanda Sanz, Ester Sanchez, Marta Marzotto, Miguel Calabuig, Sandra Torriani, and Franco Dellaglio set out to determine what differences might exist between the microbiotic bacteria in the guts of children with celiac disease compared to a healthy control group of their peers. The team conducted a denaturing gradient gel electrophoresis analysis of fecal samples from both the celiac and the control groups. They found that children with celiac disease had a more diverse profile of intestinal microbiotic bacteria than did the healthy control subjects. The children with celiac disease were characterized by the presence of Lactobacillus curvatus, Leuconostoc mesenteriodes, and Leuconostoc carnosum, whereas the members of the healthy control group were characterized by the presence of Lactobacillus casei. Conversely, the bifidobacterium population was much greater in the members of the healthy control group than among the children with celiac disease. The healthy control group showed particularly high populations of bifidobacterium adolescentis compared to the celiac patients. The team has called for more research into which populations of the various gut microbial are affected by celiac disease. This may lead to a possible role for probiotics and/or prebiotics in returning the balance of the gut microbes in those with celiac disease. FEMS Immunol Med Microbiol. 2007 Dec;51(3):562-8
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