1,721,195 research outputs found
Gliadin can Alter Tight Junctions Proteins in an In Vitro Model
No full textBackground and aim. Cytoskeleton and tight junctions play a pivotal role in maintaining the integrity of the intestinal barrier. A damage of these structures is involved in the pathogenesis of celiac disease. Our aim is to investigate the direct effect of gliadin on the tight junction proteins in an in vitro three-dimensional model. Materials and methods. Lovo multicellular spheroids were treated with digested bread wheat gliadin 500 microg/mL. At the end of the treatment morphology and structure of the spheroids were evaluated by means of light microscopy, scanning and transmission electron microscopy. The effect of gliadin on actin and the tight-junction proteins, occludin and zonula occludens-1, was evaluated by means of confocal laser microscopy. Results. The gliadin-treated spheroids developed holes and superficial blebs and showed profound ultrastrucural rearrangement and tight junction alterations. Incubation of Lovo spheroids with gliadin reduced the intracellular actin filaments and disassembled the integrity of the tight junction proteins. Conclusion. Our data obtained from a three-dimensional cell culture model demonstrate the direct noxious effect of gliadin on the cytoskeleton and tight junctions of Lovo cell line and suggest a role in the pathogenesis of celiac disease
Non-celiac gluten sensitivity : time for sifting the grain
Full text linkIn the last few years, a new nomenclature has been proposed for the disease induced by the ingestion of gluten, a protein present in wheat, rice, barley and oats. Besides celiac disease and wheat allergy, the most studied forms of gluten-related disorders characterized by an evident immune mechanism (autoimmune in celiac disease and IgE-mediated in wheat allergy), a new entity has been included, apparently not driven by an aberrant immune response: the non-celiac gluten sensitivity (NCGS). NCGS is characterized by a heterogeneous clinical picture with intestinal and extraintestinal symptoms arising after gluten ingestion and rapidly improving after its withdrawal from the diet. The pathogenesis of NCGS is largely unknown, but a mixture of factors such as the stimulation of the innate immune system, the direct cytotoxic effects of gluten, and probably the synergy with other wheat molecules, are clues for the complicated puzzle. In addition, the diagnostic procedures still remain problematic due to the absence of efficient diagnostic markers; thus, diagnosis is based upon the symptomatic response to a gluten-free diet and the recurrence of symptoms after gluten reintroduction with the possibility of an important involvement of a placebo effect. The temporary withdrawal of gluten seems a reasonable therapy, but the timing of gluten reintroduction and the correct patient management approach are have not yet been determined
Gliadin cytotoxicity and in vitro cell cultures
No full textInterest in celiac disease, a common enteropathy in Europe and the USA (1/200) caused by the dietary ingestion of gluten in susceptible subjects, has increased over the last few years. Its pathogenesis is still not completely clear, but it certainly involves immune-mediated mechanisms. Although a number of studies have been published concerning the role of T cells in inducing intestinal damage, little is known about the early stages in which gliadin (the toxic component of gluten) starts the whole process. In vitro two- and three-dimensional (multicellular spheroid) cell cultures are a simple and useful means of studying the direct cellular effects of gliadin and other "toxic" cereal peptides. Furthermore, in addition to improving our understanding of pathogenetic mechanisms, cell cultures can also be used to test modified peptides that could replace the toxic components present in the foods that celiac patients must avoid
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
- …
