Consistent alterations in faecal microbiomes of patients with primary sclerosing cholangitis independent of associated colitis
Adult
Male
0301 basic medicine
Adolescent
Norway
Cholangitis, Sclerosing
610
Middle Aged
Altered Faecal Microbiome in Psc
Gastrointestinal Microbiome
3. Good health
Cohort Studies
Feces
Young Adult
03 medical and health sciences
Germany
RNA, Ribosomal, 16S
Humans
Colitis, Ulcerative
Female
Aged
DOI:
10.1111/apt.15375
Publication Date:
2019-06-28T07:34:33Z
AUTHORS (17)
ABSTRACT
SummaryBackgroundSingle‐centre studies reported alterations of faecal microbiota in patients with primary sclerosing cholangitis (PSC). As regional factors may affect microbial communities, it is unclear if a microbial signature of PSC exists across different geographical regions.AimTo identify a robust microbial signature of PSC independent of geography and environmental influences.MethodsWe included 388 individuals (median age, 47 years; range, 15‐78) from Germany and Norway in the study, 137 patients with PSC (n = 75 with colitis), 118 with ulcerative colitis (UC) and 133 healthy controls. Faecal microbiomes were analysed by 16S rRNA gene sequencing (V1‐V2). Differences in relative abundances of single taxa were subjected to a meta‐analysis.ResultsIn both cohorts, microbiota composition (beta‐diversity) differed between PSC patients and controls (P < 0.001). Random forests classification discriminated PSC patients from controls in both geographical cohorts with an average area under the curve of 0.88. Compared to healthy controls, many new cohort‐spanning alterations were identified in PSC, such as an increase of Proteobacteria and the bile‐tolerant genus Parabacteroides, which were detected independent from geographical region. Associated colitis only had minor effects on microbiota composition, suggesting that PSC itself drives the faecal microbiota changes observed.ConclusionCompared to healthy controls, numerous microbiota alterations are reproducible in PSC patients across geographical regions, clearly pointing towards a microbiota composition that is shaped by the disease itself and not by environmental factors. These reproducibly altered microbial populations might provide future insights into the pathophysiology of PSC.
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