Background/Aim: At present, a gluten-free diet is the only efficient way to treat celiac disease (CD). The development of novel approaches lessen or counteract pathogenic effects gluten remains crucial for treatment CD. aim in this investigation was examine restorative Acetobacter ghanensis as probiotic against gliadin-induced modulation barrier integrity an intestinal epithelial cell (IEC) mod...

SCOPE Celiac disease is an autoimmune disorder caused by failure of oral tolerance against gluten in genetically predisposed individuals. The epithelial translocation of gluten-derived gliadin peptides is an important pathogenetic step; the underlying mechanisms, however, are poorly understood. Thus, we investigated the degradation and epithelial translocation of two different gliadin peptides,...

BACKGROUND AND AIMS Celiac disease (CD) is a chronic inflammatory disorder of the small intestine that is induced by dietary wheat gluten proteins (gliadins) in genetically predisposed individuals. The overgrowth of potentially pathogenic bacteria and infections has been suggested to contribute to CD pathogenesis. We aimed to study the effects of gliadin and various intestinal bacterial strains...

The lack of digestibility of certain gluten proteins is essential in the development of celiac disease (CD). Gluten proteins are remarkably resistant to luminal and brush-border proteolysis owing to their high proline and glutamine content. Consequently, large fragments remain intact after digestion exerting toxic effects. Intestinal brush-border membrane vesicles (BBMV) have been described as ...

Gluten promotes type 1 diabetes in nonobese diabetic (NOD) mice and likely also in humans. In NOD mice and in non-diabetes-prone mice, it induces inflammation in the pancreatic lymph nodes, suggesting that gluten can initiate inflammation locally. Further, gliadin fragments stimulate insulin secretion from beta cells directly. We hypothesized that gluten fragments may cross the intestinal barri...

Copolymers of sodium 4-styrene sulfonate (SS) and hydroxyethyl methacrylate (HEMA) were investigated as sequestrants of alpha-gliadin, a gluten protein, for the treatment of gluten intolerance. The interactions of alpha-gliadin with poly(SS) and poly(HEMA-co-SS) with 9 and 26 mol% SS content were studied at gastric (1.2) and intestinal (6.8) pH using circular dichroism and measurements of turbi...

BACKGROUND Celiac disease (CD) is a chronic, small intestinal inflammatory disease mediated by dietary gluten and related prolamins. The only current therapeutic option is maintenance of a strict life-long gluten-free diet, which implies substantial burden for CD patients. Different treatment regimes might be feasible, including masking of toxic celiac peptides with blocking antibodies or fragm...

BACKGROUND Intestinal exposure to gliadin leads to zonulin upregulation and consequent disassembly of intercellular tight junctions and increased intestinal permeability. We aimed to study response to gliadin exposure, in terms of barrier function and cytokine secretion, using intestinal biopsies obtained from four groups: celiac patients with active disease (ACD), celiac patients in remission ...

Searching for a mechanism underlying autoimmunity in autism, we postulated that gliadin peptides, heat shock protein 60 (HSP-60), and streptokinase (SK) bind to different peptidases resulting in autoantibody production against these components. We assessed this hypothesis in patients with autism and in those with mixed connective tissue diseases. Associated with antigliadin and anti-HSP antibod...

BACKGROUND In coeliac disease (CD) patients, the dominant DQ2-Alpha-I-gliadin peptide recognised by CD4 T cells is contained within peptide sequence 57-73 (p57-73) of Alpha-gliadin. This peptide sequence is also located within a 33-mer protease resistant gliadin fragment and therefore is likely to play an important role in the pathogenesis of CD. AIMS Our aim was to determine whether a B cell...