ArticlePloS one2011
Gliadin-mediated proliferation and innate immune activation in celiac disease are due to alterations in vesicular trafficking.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 76 citations in OpenAlex.
- Pediatric Celiac Disease Patients Show Alterations of Dendritic Cell Shape and Actin Rearrangement.International journal of molecular sciences · 2021Trial
- Refractory Celiac Disease: Nutritional Failure, Immune Dysregulation, and Lymphomagenesis.Nutrients · 2026Review
- Immune cell dynamics and mechanisms of epithelial injury in celiac disease.Frontiers in immunology · 2026Review
- Innate immune dysregulation in celiac disease and refractory celiac disease: mechanisms, management and emerging therapies.Frontiers in immunology · 2026Review
- From gluten to therapeutics: molecular mechanisms of celiac disease and emerging alternatives to the gluten-free diet.Frontiers in pharmacology · 2026Review
- Gastrointestinal tract, its pathophysiology andWorld journal of gastroenterology · 2025Review
- Article
- Assessment of salivary microbiota profile as a potential diagnostic tool for pediatric celiac disease.Scientific reports · 2024Article
- The Combination of Gold and Silver Food Nanoparticles with Gluten Peptides Alters the Autophagic Pathway in Intestinal Crypt-like Cells.International journal of molecular sciences · 2023Article
- The protective role ofFrontiers in medicine · 2023Article
- Article
- Inflammation Is Present, Persistent and More Sensitive to Proinflammatory Triggers in Celiac Disease Enterocytes.International journal of molecular sciences · 2022Article
- Development of a Sequence Searchable Database of Celiac Disease-Associated Peptides and Proteins for Risk Assessment of Novel Food Proteins.Frontiers in allergy · 2022Article
- Interplay Between Gluten, HLA, Innate and Adaptive Immunity Orchestrates the Development of Coeliac Disease.Frontiers in immunology · 2021Review
- Ancestral Wheat Types Release Fewer Celiac Disease Related T Cell Epitopes than Common Wheat upon Ex Vivo Human Gastrointestinal Digestion.Foods (Basel, Switzerland) · 2020Article
- mTOR sustains inflammatory response in celiac disease.Scientific reports · 2020Article
- Iron Absorption in Celiac Disease and Nutraceutical Effect of 7-Hydroxymatairesinol. Mini-Review.Molecules (Basel, Switzerland) · 2020Review
- Coeliac Disease Pathogenesis: The Uncertainties of a Well-Known Immune Mediated Disorder.Frontiers in immunology · 2020Review
- Transglutaminase 2 and Transglutaminase 2 Autoantibodies in Celiac Disease: a Review.Clinical reviews in allergy & immunology · 2019Review
- Introducing tumor necrosis factor as a prominent player in celiac disease and type 1 diabetes mellitus.Gastroenterology and hepatology from bed to bench · 2019Article
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
objectivesDamage to intestinal mucosa in celiac disease (CD) is mediated both by inflammation due to adaptive and innate immune responses, with IL-15 as a major mediator of the innate immune response, and by proliferation of crypt enterocytes as an early alteration of CD mucosa causing crypts hyperplasia. We have previously shown that gliadin peptide P31-43 induces proliferation of cell lines and celiac enterocytes by delaying degradation of the active epidermal growth factor receptor (EGFR) due to delayed maturation of endocytic vesicles. IL-15 is increased in the intestine of patients affected by CD and has pleiotropic activity that ultimately results in immunoregulatory cross-talk between cells belonging to the innate and adaptive branches of the immune response. Aims of this study were to investigate the role of P31-43 in the induction of cellular proliferation and innate immune activation. METHODS/PRINCIPAL
findingsCell proliferation was evaluated by bromodeoxyuridine (BrdU) incorporation both in CaCo-2 cells and in biopsies from active CD cases and controls. We used real-time PCR to evaluate IL-15 mRNA levels and FACS as well as ELISA and Western Blot (WB) analysis to measure protein levels and distribution in CaCo-2 cells. Gliadin and P31-43 induce a proliferation of both CaCo-2 cells and CD crypt enterocytes that is dependent on both EGFR and IL-15 activity. In CaCo-2 cells, P31-43 increased IL-15 levels on the cell surface by altering intracellular trafficking. The increased IL-15 protein was bound to IL15 receptor (IL-15R) alpha, did not require new protein synthesis and functioned as a growth factor.
conclusionIn this study, we have shown that P31-43 induces both increase of the trans-presented IL-15/IL5R alpha complex on cell surfaces by altering the trafficking of the vesicular compartments as well as proliferation of crypt enterocytes with consequent remodelling of CD mucosa due to a cooperation of IL-15 and EGFR.
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