Gliadin-dependent UPR induction directly triggers the expression of TG2 and pro-inflammatory cytokines, dysregulates intestinal permeability, and reduces CFTR expression in intestinal epithelial cells of celiac disease patients - Monzani, Romina; Gagliardi, Mara; Saverio, Valentina; Clemente, Nausicaa; Monzani, Alice; Rabbone, Ivana; Nigrelli, Francesca; Pellizzaro, Samuele; Ferrario, Emanuele; Saettone, Silvia; Pagano, Nico; De Leo, Luigina; et al. (Biology direct, 2025)
Keywords: Animals; Antigens; Autoimmune diseases; Biopsy; Caco-2 Cells; Celiac disease; Celiac Disease - metabolism; Chemical chaperone; Complications and side effects; Cystic fibrosis; Cystic Fibrosis Transmembrane Conductance Regulator - genetics; Cystic Fibrosis Transmembrane Conductance Regulator - metabolism; Cytokines; Cytokines - genetics; Cytokines - metabolism; Development and progression; Digestive system; Endoplasmic reticulum; Endoplasmic Reticulum Stress; Epithelial cells; Epithelial Cells - metabolism; Epithelium; Gastrointestinal tract; Gliadin; Gliadin - metabolism; Gluten; GTP-Binding Proteins - genetics; GTP-Binding Proteins - metabolism; Health aspects; Homeostasis; Humans; IEC; Immune response; Immune system; Inflammation; Intestinal Barrier Function; Intestinal Mucosa - metabolism; Intestine; Male; Membrane proteins; Mice; Molecular modelling; Pathogenesis; Peptides; Permeability; Protein folding; Protein Glutamine gamma Glutamyltransferase 2; Proteins; Small intestine; Therapeutic targets; Transcription factors; Transferases; Transglutaminases - genetics; Transglutaminases - metabolism; Unfolded Protein Response; UPR; Western blotting; γ-Interferon; Italy; CD; Chemical chaperone; IEC; UPR; Endoplasmic reticulum stress