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Neither black nor white: do altered intestinal microbiota reflect chronic liver disease severity?
  1. Felix Goeser1,2,
  2. Philipp Münch3,4,
  3. Till Robin Lesker3,5,
  4. Philipp Ludwig Lutz1,2,
  5. Benjamin Krämer1,2,
  6. Dominik J Kaczmarek1,
  7. Claudia Finnemann1,2,
  8. Hans Dieter Nischalke1,
  9. Robert Geffers6,
  10. Marijo Parcina7,
  11. Alice McHardy3,4,
  12. Christian Strassburg1,
  13. Achim Hoerauf2,7,
  14. Jacob Nattermann1,2,
  15. Isabelle Bekeredjian-Ding2,8,
  16. Ulrich Spengler1,2
  1. 1Department of Internal Medicine I, University Hospital Bonn, Bonn, Germany
  2. 2Partner Site Bonn/Cologne, German Center for Infection Research (DZIF), Bonn, Germany
  3. 3Computational Biology for Infection Research, Helmholtz-Zentrum fur Infektionsforschung GmbH, Braunschweig, Niedersachsen, Germany
  4. 4Partner Site Hannover-Braunschweig, German Centre for Infection Research (DZIF), Braunschweig, Germany
  5. 5Microbial Immune Regulation, Helmholtz-Zentrum fur Infektionsforschung GmbH, Braunschweig, Niedersachsen, Germany
  6. 6Institute for Genomanalytik, Helmholtz Centre for Infection Research, Braunschweig, Germany
  7. 7Institute of Medical Microbiology, Immunology and Parasitology, University Hospital Bonn, Bonn, Germany
  8. 8Division of Microbiology, Paul-Ehrlich-Institut, Langen, Hessen, Germany
  1. Correspondence to Dr Felix Goeser, Department of Internal Medicine I, University Hospital Bonn, Bonn D-53217, Germany; felix.goeser{at}ukbonn.de

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In their outstanding study, Wei et al1 compared the intestinal microbiota (IM) of well-defined autoimmune hepatitis (AIH) patients to healthy controls. They reported significantly reduced IM alpha diversity and disparate IM compositional heterogeneity (beta diversity) with enrichment of Streptococcus, Veillonella, Klebsiella and Lactobacillus in AIH. The excellent achievement of this study is to have characterised the IM of untreated patients with AIH. However, differentiation between IM changes caused by AIH in particular and by chronic liver disease (CLD) in general was not possible because this study lacked a control group with CLD other than AIH.

In a pilot study, we analysed the IM of patients with CLD of mixed aetiology in comparison to healthy controls to clarify alterations across different stages of CLD (table 1 and online supplementary data). In contrast to the study by Wei et al, patients with recent intake of antibiotics were excluded. Additionally, only patients on proton pump inhibitors (PPIs), which are frequently taken by patients with CLD, were included to avoid a bias due to mixed PPI use, because PPI can alter the IM, in particular, the abundance of Veillonellaceae and Streptococcaceae.2 Based on investigations of normalised relative reads (n-RR) per IM taxon as well as IM alpha-diversity and beta-diversity analyses, we detected Veillonella …

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Footnotes

  • JN, IB-D and US are joint senior authors.

  • Contributors Concept and design: FG, JN, IB-D and US; collection of patient-derived samples: FG, PLL and DJK; establishment of procedures/protocols and performance of experiments: FG, BK, CF, HDN, RG and MP; analysis of data: FG, PM, TRL and US; interpretation and integration of data: FG, PM, TRL, AMcH, JN, IB-D and US; writing of the manuscript: FG, PLL, JN, IB-D and US; supervision: AMcH, CS, AH, JN, IB-D and US; all authors proofread the final version of the manuscript.

  • Funding FG received a 'clinical leave stipend' by the German Center for Infection Research between August 2014 and February 2016.

  • Competing interests None declared.

  • Patient and public involvement Patients and/or the public were not involved in the design, conduct, reporting or dissemination plans of this research.

  • Patient consent for publication Not required.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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