Abstract
Celiac disease (CD) is a chronic autoimmune disease characterized by an immune-triggered enteropathy upon gluten intake. The only current treatment available is lifelong Gluten Free Diet (GFD). Several extraintestinal manifestations have been described in CD, some affecting the oral mucosa. Thus, we hypothesized that oral mucosa could potentially be a target for novel biomarkers and an administration route for CD treatment. Six de novo diagnosed and seven CD patients under GFD for at least 1 year were recruited. Non-celiac subjects (n = 8) were recruited as control group. Two biopsies of the cheek lining were taken from each subject for mRNA analysis and immunohistochemical characterization. We observed a significant decrease in the expression of epithelial junction proteins in all CD patients, indicating that oral mucosa barrier integrity is compromised. FoxP3+ population was greatly increased in CD patients, suggesting that Tregs are recruited to the damaged mucosa, even after avoidance of gluten. Amphiregulin mRNA levels from Peripheral Blood Mononuclear Cells (PBMCs) and epithelial damage in the oral mucosa correlated with Treg infiltration in all the experimental groups, suggesting that recruited Tregs might display a “repair” phenotype. Based on these results, we propose that oral mucosa is altered in CD and, as such, might have diagnostic potential. Furthermore, due to its tolerogenic nature, it could be an important target for oral immunotherapy.
Highlights
Celiac disease (CD) is characterized by an immune-mediated chronic enteropathy of the small intestine, triggered by the ingestion of gluten in genetically predisposed individuals
We have found that the oral epithelial barrier of CD patients is compromised, even when they adhere to a Gluten Free Diet (GFD)
Celiac disease is a chronic autoimmune enteropathy triggered by gluten intake
Summary
Celiac disease (CD) is characterized by an immune-mediated chronic enteropathy of the small intestine, triggered by the ingestion of gluten in genetically predisposed individuals. It is characterized by the atrophy of the villi of the small intestinal mucosa, which entails a syndrome of nutrient malabsorption [1]. CD diagnosis is currently based on several features that include, besides the HLA haplotypes, serological markers (IgA antiendomysial and/or IgA anti-tissue transglutaminase -tTG2-) and gluten-induced intestinal morphological changes. These changes have led to the Marsh classification score based on a) lymphocyte infiltrates at the intraepithelial compartment; b) crypt hyperplasia; and c) villous atrophy [5]. CD diagnosis requires a biopsy from the small intestine, a sampling technique that is invasive and entails possible complications for the patients
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