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Transcription profiling by array of human duodenum biopsies from normalized celiac patients treated with gliadin

ABSTRACT: Study of the effects of re-exposure to gliadin of intestinal biopsies from normalized celiac patients (>2 years on gluten free diet). Comparison of the expresson profile in biopsy portions incubated with 10ug/ml gliadin versus without gliadin for 4 hours.

ORGANISM(S): Homo sapiens

SUBMITTER: Jose Ramon Bilbao

PROVIDER: E-MEXP-1823 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Long-term and acute effects of gliadin on small intestine of patients on potentially pathogenic networks in celiac disease.

Castellanos-Rubio Ainara A Santin Izortze I Martin-Pagola Ainhoa A Irastorza Iñaki I Castaño Luis L Vitoria Juan Carlos JC Bilbao Jose Ramon JR

Autoimmunity 20100301 2

Celiac disease (CD) is a complex, immune-mediated intolerance to gliadin that develops in genetically susceptible individuals. Although the main driving force of the disease is an aberrant autoimmune response, several other pathogenic mechanisms, many still unidentified, are also involved. In order to describe at a network level the alterations provoked by a gliadin insult on the intestinal mucosa of patients, we compared the expression profiles of biopsies from 9 active and 9 treated patients ( ...[more]

PMID: 19814655

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Transcription profiling of duodenum biopsies from patients with celiac disease taken at time of diagnosis or after two years of a gluten free diet

Project description:Study on the effects of long term, dietary, consumption of gliadin (gluten) in patients with celiac disease. Comparison of expression profiles of biopsies from normalized patients treated with gluten-free diet >2 years (FU-follow-up samples) versus biopsies from patients with active disease (Dx-at diagnosis samples)

2009-06-01 | E-MEXP-1828 | biostudies-arrayexpress

Chronic inflammation permanently reshapes tissue-resident immunity in celiac disease

Project description:Chronic inflammation driven by persistent antigenic challenge with dietary gluten permanently reshapes the tissue-resident TCRgd+ intraepithelial lymphocyte compartment in patients with celiac disease.

2018-12-12 | GSE123649 | GEO

Genome-wide analysis of B and T cell gene expression during a six-week gluten challenge in patients with celiac disease

Project description:Dietary gluten proteins (prolamins) from wheat, rye, and barley are the driving forces behind celiac disease, an organ-specific autoimmune disorder that targets both the small intestine and organs outside the gut. In the small intestine, gluten induces inflammation and a typical morphological change of villous atrophy and crypt hyperplasia. Gut lesions improve and heal when gluten is excluded from the diet and the disease relapses when patients consume gluten. Oral immune tolerance towards gluten may be kept for years or decades before breaking tolerance in genetically susceptible individuals. Celiac disease provides a unique opportunity to study autoimmunity and the transition in immune cells as gluten breaks oral tolerance. Seventy-three celiac disease patients on a long-term gluten-free diet ingested a known amount of gluten daily for six weeks. A peripheral blood sample and intestinal biopsies were taken before and six weeks after initiating the gluten challenge. Biopsy results were reported on a continuous numeric scale that measured the villus height to crypt depth ratio to quantify gluten-induced gut mucosal injury. Pooled B and T cells were isolated from whole blood, and RNA was analyzed by DNA microarray looking for changes in peripheral B- and T-cell gene expression that correlated with changes in villus height to crypt depth, as patients maintained or broke oral tolerance in the face of a gluten challenge.

2017-01-27 | GSE87629 | GEO

Reprogramming of CTLs into natural killer-like cells in celiac disease

Project description:Celiac disease is an intestinal inflammatory disorder induced by dietary gluten in genetically susceptible individuals. The mechanisms underlying the massive expansion of interferon g–producing intraepithelial cytotoxic T lymphocytes (CTLs) and the destruction of the epithelial cells lining the small intestine of celiac patients have remained elusive. We report massive oligoclonal expansions of intraepithelial CTLs that exhibit a profound genetic reprogramming of natural killer (NK) functions. These CTLs aberrantly expressed cytolytic NK lineage receptors, such as NKG2C, NKp44, and NKp46, which associate with adaptor molecules bearing immunoreceptor tyrosine-based activation motifs and induce ZAP-70 phosphorylation, cytokine secretion, and proliferation independently of T cell receptor signaling. This NK transformation of CTLs may underlie both the self-perpetuating, gluten-independent tissue damage and the uncontrolled CTL expansion leading to malignant lymphomas in severe forms of celiac disease. Because similar changes were detected in a subset of CTLs from cytomegalovirus-seropositive patients, we suggest that a stepwise transformation of CTLs into NK-like cells may underlie immunopathology in various chronic infectious and inflammatory diseases. Keywords: NKG2C; LAK; CTL; NK receptor; IEL; Mucosal Immunity; Celiac Disease

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Expression analysis in intestinal mucosa of genes under association peaks in celiac disease

Project description:Celiac disease is a chronic immune-mediated disorder with an important genetic component. To date, there are 57 independent association signals from 39 non-HLA loci, and a total of 66 candidate genes have been proposed. We aimed to scrutinize the functional implication of 45 of those genes by analyzing their expression in the disease tissue of celiac patients (at diagnosis/treatment) compared to non-celiac controls. The sample set consisted of 15 CD children at diagnosis (on a gluten-containing diet, with CD associated antibodies, atrophy of intestinal villi and crypt hyperplasia), and the same patients in remission after being treated with GFD for >2 years (asymptomatic, antibody negative, and normalized intestinal epithelium at that time), plus 15 tissue samples from non-celiac individuals not suffering from inflammation at the time of endoscopy used as controls

2014-09-30 | E-GEOD-61849 | biostudies-arrayexpress

Gene expression assessed by genome wide hybridization bead array in T84 polarized tight monolayers after challenge with celiac disease-associated bacteria and gluten [A grav, Bmix Bmix glut]

Project description:Analysis of the influence of celiac disease-associated bacteria and gluten on intestinal epithelial cells

2017-08-26 | GSE103100 | GEO

Gene expression assessed by genome wide hybridization bead array in T84 polarized tight monolayers after challenge with celiac disease-associated bacteria and gluten [CTR glut bmix, bmix and gluten]

Project description:Analysis of the influence of celiac disease-associated bacteria and gluten on intestinal epithelial cells

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Transcriptomic Signature of Celiac show induced epithelial proliferation coupled with suppressed metabolic functions

Project description:Background and aims: Celiac disease is provoked by gluten exposure, but the resultant pathogenic process in the duodenum is not well understood. We aimed to define the core celiac transcriptomic signature and pathologic pathways in pre-treatment diagnostic duodenum biopsies. Methods: We use mRNAseq to define pre-treatment diagnostic duodenum gene expression in 54 pediatric celiac patients and non-celiac controls, and we validate our key findings in an independent cohort of 40 participants. We further define similar and divergent genes and pathways in 177 Crohn disease patients and controls. Results: We observe a marked suppression of mature epithelial metabolic functions in celiac patients, overlapping substantially with the Crohn signature. A marked adaptive immune response was noted for the up-regulated signature including interferon response, alpha-beta, and gamma-delta T-cells that overlapped to some extant with the Crohn signature. However, we identified a celiac specific signature linked to increased cell proliferation, nuclear division, and cell cycle activity that was localized primarily to the epithelia as noted by CCNB1 and Ki67 staining. Lastly, we demonstrate the utility of the transcriptomic date to correctly classify disease or healthy states in the discovery and validation cohorts. Conclusion: Our data provide insights into celiac pathogenesis and can stimulate new approaches to address this highly prevalent condition.

2020-04-10 | GSE131705 | GEO

Human gut derived-organoids as model to study gluten response and effects of microbiota bioproducts in celiac disease

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Gluten induces rapid reprogramming of natural memory αβ and γδ intraepithelial T cells to induce cytotoxicity in celiac disease

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