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

被引:37
作者
Hedin, Charlotte R. [1 ]
van der Gast, Christopher J. [2 ]
Stagg, Andrew J. [3 ]
Lindsay, James O. [3 ,4 ]
Whelan, Kevin [5 ]
机构
[1] Karolinska Univ Hosp, Dept Med, Stockholm, Sweden
[2] Manchester Metropolitan Univ, Sch Healthcare Sci, Manchester, Lancs, England
[3] Queen Mary Univ London, Ctr Immunobiol, Blizard Inst, London, England
[4] Barts Hlth NHS Trust, Dept Gastroenterol, London, England
[5] Kings Coll London, Fac Life Sci & Med, Diabet & Nutr Sci Div, London, England
关键词
Crohn's disease; microbiome; Faecalibacterium prausnitzii; siblings; inflammatory bowel disease; bifidobacteria; CROHNS-DISEASE; INTESTINAL MICROBIOME; ULCERATIVE-COLITIS; DIVERSITY; RISK; MICE; ASSOCIATION; TWINS; PHENOTYPES; PATTERNS;
D O I
10.1080/19490976.2017.1284733
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
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.
引用
收藏
页码:359 / 365
页数:7
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