BackgroundCeliac disease (CD) is an autoimmune disorder of the small intestine which is triggered by dietary gluten in genetically predisposed (HLA-DQ2/DQ8 positive) individuals. Only a fraction of HLA-DQ2/DQ8 positive individuals develop CD indicating that other factors have a role in the disorder. Several studies have addressed intestinal microbiota aberrancies in pediatric CD, but the results are inconsistent. Previously, we demonstrated that pediatric CD patients have lower duodenal expression of TLR2 and higher expression of TLR9 as compared to healthy controls (HC) indicating that microbiota may have a role in CD.MethodsWe used bacterial phylogenetic microarray to comprehensively profile the microbiota in duodenal biopsies of CD (n = 10) and HC (n = 9) children. The expression of selected mucosa-associated genes was assessed by qRT-PCR in CD and HC children and in treated CD adults (T-CD, n = 6) on gluten free diet.ResultsThe overall composition, diversity and the estimated microbe associated molecular pattern (MAMP) content of microbiota were comparable between CD and HC, but a sub-population profile comprising eight genus-like bacterial groups was found to differ significantly between HC and CD. In HC, increased TLR2 expression was positively correlated with the expression of tight junction protein ZO-1. In CD and T-CD, the expression of IL-10, IFN-g and CXCR6 were higher as co5mpared to HC.ConclusionsThe results suggest that microbiota and altered expression of mucosal receptors have a role in CD. In CD subjects, the increased expression of IL-10 and IFN-g may have partly resulted from the increased TLR9 expression and signaling.

Altered gene expression of TLR2, TLR9, and TOLLIP in small intestinal biopsies in celiac disease suggests that microbiota-associated factors may be important in the development of the disease.

Oral mucosal lesions or dental enamel defects may be the only presenting features of coeliac disease. A series of 128 patients with coeliac disease (CD) on a gluten-free diet (GFD), 8 patients with a newly diagnosed CD, and 30 healthy controls participated in a clinical and histopathological study of their oral mucosa. Oral mucosal lesions occurred in 71/128 GFD-treated CD patients. in 4/8 untreated and in 10/30 controls, and oral symptoms in 85/128, in 6/8 and in 10/30, respectively. Five CD patients had aphthous ulcers. Moderate to severe lymphocytic inflammation occurred in 36/117 and in 14/117 of the biopsy specimens of GFD-treated CD patients, in 1/8 and 2/8 of untreated CD patients, and in 3/30 and in 1/30 of controls, respectively. Intraepithelial T-cells were significantly more frequent in GFD-treated CD patients than in controls. There was no difference between untreated CD patients and controls. In the lamina propria of the GFD-treated CD patients, T-cells were more frequent than in the other groups. Mast cells were significantly more frequent in patients with GFD-treated CD. Nine GFD-treated CD patients had raised serum endomysium IgA antibody titres, although five of them reported to follow a strict GFD. A lack of strict compliance with a GFD may be related to the high prevalence of oral changes and symptoms. In addition, T-cell infiltration in the oral mucosa tends to increase with a longer duration of CD, independent of GFD-treatment. Clinically, it is important to study the oral cavity of patients suspected of having CD where the only clue to the disease may reside, since no less than 66% of the patients in this study had oral symptoms.

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