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Puslapis 1 nuo 381 rezultatus
Anti gliadin antibodies (AGA IgG) related to peripheral inflammation in schizophrenia.
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Altered immune function and inflammation are seen in schizophrenia, however, peripheral inflammatory markers are not consistently elevated in all people, suggesting inflammation may be present only in a subgroup. We measured TNF-α and IL-Iβ in 100 people with schizophrenia or schizoaffective
Autoantibody screen in inflammatory myopathies high prevalence of antibodies to gliadin.
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BACKGROUND
Inflammatory myopathies (IM) are associated with autoimmune diseases.
OBJECTIVE
To evaluate the titers of auto-antibodies specific to various autoimmune diseases in patients with IM compared with controls.
METHODS
Sera from 99 IM patients and 100 healthy controls were tested for
Observations of the time-course of the inflammatory response of rectal mucosa to gliadin challenge in gluten-sensitive subjects.
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Expression of endothelial adhesion molecules is a key factor in localizing inflammatory processes. We have evaluated the time-course expression of E-selectin, ICAM-1, and VCAM-1 in rectal mucosae from coeliac patients (CD) with T-lymphocyte sensitization to wheat (gliadin) protein. Ten treated,
Antibody (IgG, IgA, and IgM) to baker's yeast (Saccharomyces cerevisiae), yeast mannan, gliadin, ovalbumin and betalactoglobulin in monozygotic twins with inflammatory bowel disease.
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To assess whether dietary antigens play a role in inflammatory bowel disease, 26 monozygotic twin pairs with inflammatory bowel disease and 52 healthy controls were investigated for serum antibodies (IgA, IgG, IgM) against ovalbumin, betalactoglobulin, gliadin, whole yeast (Saccharomyces cerevisiae)
Ascorbate-dependent decrease of the mucosal immune inflammatory response to gliadin in coeliac disease patients.
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BACKGROUND
The IL-15/NF-κB axis has an important role in coeliac disease (CD) and may represent a molecular target for immunomodulation. Ascorbate (vitamin C) is known to show inhibitory effects on NF-κB. Therefore, we studied if ascorbate supplementation to gliadin gliadin-stimulated biopsy culture
Modulatory Effect of Gliadin Peptide 10-mer on Epithelial Intestinal CACO-2 Cell Inflammatory Response.
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Celiac Disease (CD) is a chronic inflammatory enteropathy, triggered in genetically susceptible individuals by dietary gluten. Gluten is able to elicit proliferation of specific T cells and secretion of inflammatory cytokines in the small intestine. In this study we investigated the possibility that
Effect of anti-gliadin IgY antibody on epithelial intestinal integrity and inflammatory response induced by gliadin.
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BACKGROUND
Pepsin-trypsin resistant gliadin (PT-gliadin) promotes intestinal tissue inflammation and increases paracellular permeability of immunogenic gliadin peptides into the lamina propria. This leads to the complications seen in the pathogenesis of celiac disease (CD). In this study, specific
Dietary glycosaminoglycans interfere in bacterial adhesion and gliadin-induced pro-inflammatory response in intestinal epithelial (Caco-2) cells.
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Dietary components may have an important role in maintaining a balanced gut microbiota composition. Celiac disease is an autoimmune enteropathy caused by gliadins, and has been associated with a reduced proportion of Bifidobacterium in gut microbiota. This study evaluates the influence of
Single-chain recombinant HLA-DQ2.5/peptide molecules block α2-gliadin-specific pathogenic CD4+ T-cell proliferation and attenuate production of inflammatory cytokines: a potential therapy for celiac disease.
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Celiac disease (CD) is a disorder of the small intestine caused by intolerance to wheat gluten and related proteins in barley and rye. CD4(+) T cells have a central role in CD, recognizing and binding complexes of HLA-DQ2.5 bearing gluten peptides that have survived digestion and that are deamidated
Sensitization to and Challenge with Gliadin Induce Pancreatitis and Extrapancreatic Inflammation in HLA-DQ8 Mice: An Animal Model of Type 1 Autoimmune Pancreatitis.
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OBJECTIVE
The aim of this study was to establish a pathogenetic mechanism of pancreatitis in celiac disease and IgG4-related disease using gluten-sensitive human leukocyte antigen (HLA)-DQ8 transgenic mice.
METHODS
Transgenic mice expressing HLA-DQ8 genes were utilized. Control mice were not
Green Tea Polyphenols Mitigate Gliadin-Mediated Inflammation and Permeability in Vitro.
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Green tea, a polyphenol-rich beverage, has been reported to mitigate a number of inflammatory and hypersensitivity disorders in laboratory models, and has been shown to moderate pathways related to food allergies in vitro. The present study investigates the impact of decaffeinated green tea extract
Involvement of gliadin, a component of wheat gluten, in increased intestinal permeability leading to non-steroidal anti-inflammatory drug-induced small-intestinal damage.
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Gliadin, a component of wheat gluten known to be an important factor in the etiology of celiac disease, is related to several other diseases through its enhancing effect on intestinal paracellular permeability. We investigated the significance of gliadin in non-steroidal anti-inflammatory drug
Bifidobacteria inhibit the inflammatory response induced by gliadins in intestinal epithelial cells via modifications of toxic peptide generation during digestion.
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Celiac disease (CD) is a chronic enteropathy triggered by intake of gliadin, the toxic component of gluten. This study aims at evaluating the capacity of different Bifidobacterium strains to counteract the inflammatory effects of gliadin-derived peptides in intestinal epithelial (Caco-2) cells. A
A Probiotic Preparation Hydrolyzes Gliadin and Protects Intestinal Cells from the Toxicity of Pro-Inflammatory Peptides.
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Celiac disease (CD) is an autoimmune enteropathy caused by an intolerance to gluten proteins. It has been hypothesized that probiotic bacteria may exert beneficial effects by modulating inflammatory processes and by sustaining peptide hydrolysis at the intestinal level. This study aims at evaluating
Gliadin does not induce mucosal inflammation or basophil activation in patients with nonceliac gluten sensitivity.
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OBJECTIVE
Nonceliac gluten-sensitive (NCGS) patients report intestinal and extra-intestinal symptoms shortly after ingesting gluten; these symptoms disappear on gluten-free diets, although these patients have no serologic markers of celiac disease or intestinal damage. In fact, there is no evidence
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