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We read with interest the study by Clooney et al, which identified determinants of microbiome variance in inflammatory bowel disease (IBD).1 Despite Crohn’s disease (CD) explaining most variance, most of the faecal microbiota variation was unexplained as previously described on population level.2 CD affects the entire gut, but most studies use stool samples as a proxy for the colonic environment.3 The small intestinal microbiome differs from stool and both vertical (proximal to distal) and horizontal (luminal to mucosal) gradients exist,4 but is generally understudied, especially in CD.
Recently, we showed differences between the duodenal microbiota of healthy volunteers (HV) and functional dyspepsia (FD) patients,5 which may play a role in the pathogenesis of FD.6 Both aseptic duodenal and ileal samples (brush and biopsy)7 were collected during concurrent upper and lower endoscopy in patients with CD (see online supplemental methods). History of intestinal surgery, use of acid (proton pump inhibitors, PPIs) or immunosuppression (IS) and presence of macroscopic (erosions/ulcers) and/or microscopic inflammation were recorded. Alpha diversity was compared between sampling types (biopsy/brush), groups and treatments (PPI/IS). Genera abundance profiles were compared along vertical (duodenum/ileum) and horizontal (brush/biopsy) gradients with correction …
Contributors LW: study concept and design, data collection, analysis and interpretation of data, drafting of the manuscript and statistical analysis. RYT and MC: data collection, analysis and interpretation of data, and revision of the manuscript. AO, LR and CV: data collection and revision of the manuscript. JS, MF and SV: study concept and design, and revision of the manuscript. TV and JR: study concept and design, analysis and interpretation of data, revision of the manuscript and study supervision.
Funding LW and TV are supported by the Flanders Research Foundation (FWO Vlaanderen) through a doctoral fellowship (1190619N) and senior clinical research mandate (1830517N). RYT is supported by an FWO postdoctoral fellowship (1234321N). Jan Tack is supported by a Methusalem grant of KU Leuven (EZX-C9725-METH/14/05). The Raes lab is supported by KU Leuven, the Rega Institute and VIB. This research was funded by a grant of the Belgian IBD Research group (BIRD).
Competing interests None declared.
Provenance and peer review Not commissioned; externally peer reviewed.
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