Duodenal microbiota composition and mucosal homeostasis in pediatric celiac disease
1 Department of Veterinary Biosciences, University of Helsinki, P.O. Box 66, Helsinki FI-00014, Finland
2 Department of Pediatrics, University of Turku and Turku University Central Hospital, P.O. Box 52, Turku 20521, Finland
3 Functional Foods Forum, 20014 University of Turku, Turku, Finland
4 Laboratory of Microbiology, Wageningen University, Dreijenplein 10, Wageningen 6703 HB, The Netherlands
5 Department of Internal Medicine, Turku University Central Hospital, P.O. Box 52, Turku 20521, Finland
6 Haartman Institute, University of Helsinki, P.O. Box 21, Helsinki FI-00014, Finland
BMC Gastroenterology 2013, 13:113 doi:10.1186/1471-230X-13-113Published: 11 July 2013
Celiac 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.
We 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.
The 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.
The 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.