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Introduction Inflammation in Crohn's disease (CD) is driven by the intestinal microbiota, however, microbial manipulation with prebiotics is ineffective in treating active disease.1 Siblings of patients are at risk of developing CD, and some share aspects of the CD phenotype including raised faecal calprotectin (FC) and dysbiosis. Prebiotics may alter these risk markers. Methods Patients with inactive CD (n¼19, CD activity index <150) and 12 unaffected siblings ingested 15 g/d of fructo-oligosaccharide/ inulin (FOS) for 3 weeks. FC (enzyme-linked immunosorbant assay) and faecal microbiota (quantitative PCR targeting 16S ribosomal RNA (rRNA) genes, quantified relative to representative bacterial 16S rRNA genes) were measured at baseline and follow-up. Nonparametric statistical analyses were performed, and values presented as medians.Results In patients and siblings, Bifidobacteria and Bifidobacterium longum increased post-FOS. In siblings but not patients, Bifidobacterium adolescentis and Roseburia spp. also increased (Abstract PMO-237 table 1). Compared with patients, siblings had a greater median percentage point change in Bifidobacteria (+14.6% vs +0.4%, p¼0.028), B adolescentis (+1.1% vs 0.0% p¼0.006) and Roseburia spp. (+1.5% vs À0.1% p¼0.004). Of those with raised FC at baseline, it decreased post-FOS in only 7/19 patients (37%), compared with 4/5 (80%) siblings (p¼0.142). The change in FC was significantly negatively correlated with baseline FC in siblings (r¼À0.715, p¼0.009) but positively correlated with baseline FC in patients (r¼+0.352, p¼0.140).

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