Viscoelastic properties of wheat gluten in a molecular dynamics study.

Wheat (Triticum spp.) gluten consists mainly of intrinsincally disordered storage proteins (glutenins and gliadins) that can form megadalton-sized networks. These networks are responsible for the unique viscoelastic properties of wheat dough and affect the quality of bread. These properties have not yet been studied by molecular level simulations. Here, we use a newly developed α-C-based coarse-grained model to study ∼ 4000-residue systems. The corresponding time-dependent properties are studied through shear and axial deformations. We measure the response force to the deformation, the number of entanglements and cavities, the mobility of residues, the number of the inter-chain bonds, etc. Glutenins are shown to influence the mechanics of gluten much more than gliadins. Our simulations are consistent with the existing ideas about gluten elasticity and emphasize the role of entanglements and hydrogen bonding. We also demonstrate that the storage proteins in maize and rice lead to weaker elasticity which points to the unique properties of wheat gluten.

Sensibilidad al gluten no celíaca / Non-celiac Gluten sensitivity

Introducción: La sensibilidad al gluten no celíaca es una afección emergente descrita en la última década, mediada por mecanismos inmunes, sin reconocido marcador serológico. Objetivo: Actualizar los conocimientos sobre esta condición, patogenia, diagnóstico y tratamiento. Métodos: Se revisaron las publicaciones en español e inglés en bases de datos de Google académico, PubMed, Scielo y Latindex desde el 2014 hasta el 20 agosto 2018. Resultados: Se trata de una afección no alérgica ni autoinmune. Se analiza su repercusión en niños y adultos. La epidemiología no está establecida, su presencia varía entre 6-10 por ciento, con predominio femenino/masculino 3:1. Se revisaron los criterios sobre la patogenia relacionados con las prolaminas de cereales tóxicos, carbohidratos de cadena corta fermentable e inhibidores de amilasa y tripsina. Se evaluaron los síntomas clínicos (intestinales y extraintestinales) y analizaron los argumentos del diagnóstico definitivo y diferencial con otras enfermedades desencadenadas por gluten. La dieta sin gluten representa la única opción terapéutica. Los síntomas desaparecen con su supresión y reaparecen con su reintroducción. Consideraciones finales: La sensibilidad al gluten no celíaca es una entidad de nueva aparición con participación de procesos inmunes y patogenia sustentada por distintos mecanismos con síntomas intestinales y extraintestinales relacionados con consumo de gluten. El diagnóstico no debe ser por exclusión del gluten, sino evaluación clínica, pues no existe diagnóstico serológico. Hay otras afecciones con similares manifestaciones como enfermedad celíaca, alergia al gluten, síndrome intestino irritable y enteritis linfocítica, con las que se debe hacer diagnóstico diferencial(AU)

Introduction: Non-celiac gluten sensitivity (SGNC, by its acronyms in Spanish) is an emerging condition of the last decade, which is mediated by immune mechanisms without a recognized serological marker. Objective: To update knowledge on SGNC, its pathogenesis, diagnostic and treatment. Methods: Publications in Spanish and English were reviewed in Google scholar, PubMed, SciELO and Latindex databases from 2014 to August 20, 2018. Results: Information about the description of SGNC as a non-allergic or autoimmune condition and impact on children and adults is updated. Epidemiology is not established, although recent studies report that it varies between 6 to 10 percent, with predominance of female / male 3:1. The criteria for the pathogenesis related to the prolamines of toxic cereals, fermentable short chain carbohydrates (FODMAPs) and amylase and trypsin inhibitors are reviewed. The clinical symptoms (intestinal and extraintestinal) were evaluated and it was analyzed the argument established for the diagnosis of certainty and differential with other diseases triggered by gluten, especially celiac disease. The gluten-free diet represents the only treatment option. The symptoms disappear with gluten suppression and reappear when re-introducing it. Final Considerations: SGNC is a new entity mediated by an immune mechanism with pathogenesis supported by different mechanisms with intestinal and extra intestinal symptoms related to gluten consumption. The diagnosis should not be by exclusion of foods that contain gluten, but by clinical evaluation since there is not serological diagnosis. To know better on it is of interest due to other conditions, such as celiac disease, gluten allergy, irritable bowel syndrome and lymphocytic enteritis, which should be made by differential diagnosis(AU)

High-molecular-weight glutenin subunit-deficient mutants induced by ion beam and the effects of Glu-1 loci deletion on wheat quality properties.

BACKGROUND: High-molecular-weight glutenin subunits (HMW-GSs) play a critical role in determining the viscoelastic properties of wheat. Mutations induced by ion beam radiation have been applied to improve the yield and quality of crop. In this study, HMW-GS-deficient mutant lines were selected and the effects of Glu-1 loci deletion on wheat quality properties were illustrated according to the analysis of dry seeds of common wheat (Triticum aestivum L.) Xiaoyan 81 treated with a nitrogen ion beam. RESULTS: Three HMW-GS-deficient mutant lines were obtained and then detected by sodium dodecyl sulfate polyacrylamide gel electrophoresis. Large-chromosome-fragment deletion resulted in specific deficiencies, and the deleted region sizes were determined using molecular markers. Agronomic characters, quantity and proportion of glutenins and dough microstructure of the deletion lines all proved to be quite different from those of wild-type Xiaoyan 81. Analysis of quality properties suggested that GluA1(-) had superior property parameters, while GluB1(-) and GluD1(-) both showed a significant decrease in quality properties compared with Xiaoyan 81. CONCLUSION: The effects of the three Glu-1 loci on flour and dough quality-related parameters should be Glu-D1 > Glu-B1 > Glu-A1. Ion beam radiation can be used as a mutagen to create new crop mutants.

Are transglutaminase 2 inhibitors able to reduce gliadin-induced toxicity related to celiac disease? A proof-of-concept study.

PURPOSE: Celiac disease is an autoimmune-mediated enteropathy characterized by adaptive and innate immune responses to dietary gluten in wheat, rye and barley in genetically susceptible individuals. Gluten-derived gliadin peptides are deamidated by transglutaminase 2 (TG2), leading to an immune response in the small-intestinal mucosa. TG2 inhibitors have therefore been suggested as putative drugs for celiac disease. In this proof-of-concept study we investigated whether two TG2 inhibitors, cell-impermeable R281 and cell-permeable R283, can prevent the toxic effects of gliadin in vitro and ex vivo. METHODS: Intestinal epithelial Caco-2 cells were treated with peptic-tryptic-digested gliadin (PT-gliadin) with or without TG2 inhibitors and thereafter direct toxic effects (transepithelial resistance, cytoskeletal rearrangement, junction protein expression and phoshorylation of extracellular-signal-regulated kinase 1/2) were determined. In an organ culture of celiac-patient-derived small-intestinal biopsies we measured secretion of TG2-autoantibodies into the culture medium and the densities of CD25- and interleukin (IL) 15-positive cells, forkhead box P3 (FOXP3)-positive regulatory T cells (Tregs) and Ki-67-positive proliferating crypt cells. RESULTS: Both TG2 inhibitors evinced protective effects against gliadin-induced detrimental effects in Caco-2 cells but the cell-impermeable R281 seemed slightly more potent. In addition, TG2 inhibitor R281 modified the gluten-induced increase in CD25- and IL15-positive cells, Tregs and crypt cell proliferation, but had no effect on antibody secretion in celiac-patient-derived biopsies. CONCLUSIONS: Our results suggest that TG2 inhibitors are able to reduce certain gliadin-induced effects related to responses in vitro and ex vivo.