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Aliment Pharmacol Ther. 2019 Sep;50(5):580-589. doi: 10.1111/apt.15375. Epub 2019 Jun 28.

Consistent alterations in faecal microbiomes of patients with primary sclerosing cholangitis independent of associated colitis.

Author information

1
Kiel, Germany.
2
Hamburg, Germany.
3
Oslo, Norway.
4
Munich, Germany.
5
Homburg, Germany.
6
Warsaw, Poland.

Abstract

BACKGROUND:

Single-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.

AIM:

To identify a robust microbial signature of PSC independent of geography and environmental influences.

METHODS:

We 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.

RESULTS:

In 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.

CONCLUSION:

Compared 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.

PMID:
31250469
DOI:
10.1111/apt.15375

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