Celiac disease is classically manifested in the gastrointestinal (GI) tract but extraintestinal symptoms, such as dermatitis herpetiformis (DH), are also common. Besides several well-known shared genetic risk factors and an environmental trigger, gliadin, factors determining the clinical outcome of the disease are not known. In this study, the role of duodenal microbiota in the celiac disease outcome was studied by analyzing mucosa-associated microbiota in celiac disease patients with a variety of intestinal and extraintestinal symptoms.
Microbiota in duodenal biopsy samples obtained from 33 patients with celiac disease with GI, DH, anemia, or mixed symptoms, as well as screen-detected asymptomatic celiac disease and 18 control subjects were analyzed using PCR denaturing gradient gel electrophoresis and a subset of samples additionally by the 16S ribosomal RNA gene sequencing.
The composition and diversity of mucosal microbiota was associated with the manifestation of celiac disease when analyzed using PCR denaturing gradient gel electrophoresis and the 16S ribosomal RNA gene sequencing. The patients with celiac disease with GI symptoms or anemia had lower microbial diversity than those with DH. Moreover, the patients with GI symptoms had different intestinal microbiota composition and structure, dominated by Proteobacteria, in comparison to those with DH or control subjects (patients with dyspepsia). The relatively similar intestinal microbiota composition in the control subjects and those with DH was characterized by the high abundance of Firmicutes.
The two common outcomes of celiac disease, classical GI and extraintestinal manifestations, had marked differences on the diversity and composition of intestinal microbiota. This association suggested that intestinal microbiota may have a role in the manifestation of the disease.
Article first published online 8 March 2013
*Finnish Red Cross Blood Service, Helsinki, Finland
†Department of Gastroenterology and Alimentary Tract Surgery, Tampere University Hospital and School of Medicine, University of Tampere, Tampere, Finland
‡Pediatric Research Center, Tampere University Hospital, University of Tampere, Tampere, Finland.
Reprints: Pirjo Wacklin, PhD, Kivihaantie 7, 00310 Helsinki, Finland (e-mail: firstname.lastname@example.org).
Supported by the SalWe Research Program for IMO (Tekes—the Finnish Funding Agency for Technology and Innovation grant 648/10), the Academy of Finland, the Sigrid Juselius Foundation, and the Competitive Research Funding (EVO) of the Tampere University Hospital and Helsinki and Uusimaa Hospital district.
The authors have no conflicts of interest to disclose.
Received June 20, 2012
Accepted July 30, 2012