Celiac disease (CD) is a chronic systemic autoimmune disease by the ingestion of gluten, a storage protein present in many cereals, which affects the small intestine of individuals with a genetic predisposition. The pathological immune response is caused by a fraction of gluten called gliadin which shows toxic properties. In this study, the researchers aimed at investigating the effect of trehalose, a compound known for increasing autophagy, on counteracting gliadin cytotoxicity in the context of CD. The capability of trehalose to induce autophagy in a CD was assessed in an in vitro model based on human intestinal cells. Trehalose promoted autophagy in the intestinal cells treated with digested gliadin as well as improved cell viability. Moreover, trehalose reduced the intracellular levels of these toxic peptides. In conclusion, these results showed the beneficial effects of trehalose in a CD in vitro model, they also indicate that underlining autophagy is a molecular pathway to counteract gliadin cytotoxicity.
Trehalose modulates autophagy process to counteract gliadin cytotoxicity in an in vitro celiac disease model
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