The gut microbiota of siblings offers insights into microbial pathogenesis of inflammatory bowel disease.

Autor: Hedin CR; a Department of Medicine, Karolinska University Hospital , Solna, Stockholm., van der Gast CJ; b Manchester Metropolitan University , School of Healthcare Science , Manchester , UK., Stagg AJ; c Queen Mary University of London , Centre for Immunobiology, Blizard Institute , London , UK., Lindsay JO; c Queen Mary University of London , Centre for Immunobiology, Blizard Institute , London , UK.; d Barts Health NHS Trust , Department of Gastroenterology , London , UK., Whelan K; e King's College London , Faculty of Life Sciences & Medicine, Diabetes and Nutritional Sciences Division , London , UK.
Jazyk: angličtina
Zdroj: Gut microbes [Gut Microbes] 2017 Jul 04; Vol. 8 (4), pp. 359-365. Date of Electronic Publication: 2017 Jan 23.
DOI: 10.1080/19490976.2017.1284733
Abstrakt: Siblings of patients with Crohn's disease (CD) have elevated risk of developing CD and display aspects of disease phenotype, including faecal dysbiosis. In our recent article we have used 16S rRNA gene targeted high-throughput sequencing to comprehensively characterize the mucosal microbiota in healthy siblings of CD patients, and determine the influence of genotypic and phenotypic factors on the gut microbiota (dysbiosis). We have demonstrated that the core microbiota of both patients with CD and healthy siblings is significantly less diverse than controls. Faecalibacterium prausnitzii contributed most to core metacommunity dissimilarity between both patients and controls and between siblings and controls. Phenotype/genotype markers of CD risk significantly influenced microbiota variation between and within groups, of which genotype had the largest effect. Individuals with elevated CD-risk display mucosal dysbiosis characterized by reduced diversity of core microbiota and lower abundance of F. prausnitzii. The presence of this dysbiosis in healthy people at-risk of CD implicates microbiological processes in CD pathogenesis.
Databáze: MEDLINE