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Letter
The gut-adherent microbiota of PSC–IBD is distinct to that of IBD
  1. Mohammed Nabil Quraishi1,
  2. Martin Sergeant2,
  3. Gemma Kay2,
  4. Tariq Iqbal3,
  5. Jacqueline Chan2,
  6. Chrystala Constantinidou2,
  7. Palak Trivedi1,
  8. James Ferguson1,
  9. David H Adams1,
  10. Mark Pallen2,
  11. Gideon M Hirschfield1
  1. 1 National Institute for Health Research (NIHR) Birmingham, Liver Biomedical Research Unit, Institute of Immunology and Immunotherapy, University of Birmingham, Birmingham, UK
  2. 2 Department of Microbiology and Infection, University of Warwick, Warwick, UK
  3. 3 Department of Gastroenterology, Queen Elizabeth Hospital Birmingham, Birmingham, UK
  1. Correspondence to Dr G M Hirschfield, Centre for Liver Research, Institute of Immunology and Immunotherapy, Wolfson Drive, University of Birmingham, Birmingham, B15 2TT, UK; g.hirschfield{at}bham.ac.uk

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Primary sclerosing cholangitis–IBD (PSC–IBD) is an inflammatory autoimmune hepato–biliary–enteric disease in which it is predicted that gut microbiota have potential pathophysiological effects, relevant to disease initiation and outcome. The recent article by Kummen et al 1 who reported that the gut microbiota in PSC is distinct compared with those from healthy controls and patients with UC without liver disease, is therefore of interest. However, it remains unclear if these alterations in the gut microbiota are a cause or an effect of liver disease, and there remains a challenging task to link dysbiosis with disease pathogenesis, as well as clarify whether faecal microbiota are entirely representative of communities of mucosa-associated bacteria, which might uniquely interact with immune and epithelial cells.

Nevertheless Kummen et al notably demonstrated that the Veillonella genus showed a marked increase in PSC–IBD, in comparison with both healthy controls and patients with UC alone. Given interest in the mechanism of lymphocyte tracking between the bowel and liver …

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Footnotes

  • Contributors MNQ, THI, DHA, MP and GMH initiated and planned the study. MNQ, MS, GK, JC, CC contributed to collection of samples, laboratory preparations and post-sequencing data processing. MS and GK performed the statistical analyses and interpreted the data. MNQ wrote the first draft of the letter; GMH revised it to the point of submission. All authors contributed to reviewing and approving the final submission. GMH is the guarantor of the study.

  • Funding MNQ, PJT, DHA and GMH are supported by the NIHR Birmingham Liver Biomedical Research Unit. This article presents independent research funded by NIHR.

  • Disclaimer The views expressed are those of the authors and not necessarily those of the NHS, the NIHR or the Department of Health.

  • Competing interests None declared.

  • Ethics approval Samples were collected by the Human Biomaterials Resource Centre (HBRC). This is a Human Tissue Authority (HTA) licensed human sample biorepository (HTA research licence 12358).

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

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