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The impact of Crohn's disease genes on healthy human gut microbiota: a pilot study
  1. Christopher Quince1,
  2. Elin E Lundin2,
  3. Anna N Andreasson3,4,
  4. Dario Greco5,
  5. Joseph Rafter5,
  6. Nicholas J Talley6,
  7. Lars Agreus3,
  8. Anders F Andersson7,
  9. Lars Engstrand2,
  10. Mauro D'Amato5
  1. 1 School of Engineering, University of Glasgow, Glasgow, UK
  2. 2 Science for Life Laboratory, Department of Microbiology Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden
  3. 3 Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden
  4. 4 Stress Research Institute, Stockholm University, Stockholm, Sweden
  5. 5 Department of Biosciences and Nutrition, Karolinska Institutet, Stockholm, Sweden
  6. 6 Department of Medicine, University of Newcastle, Callaghan, New South Wales, Australia
  7. 7 Science for Life Laboratory, Division of Gene Technology, School of Biotechnology, KTH Royal Institute of Technology, Stockholm, Sweden
  1. Correspondence to Dr Mauro D'Amato, Department of Biosciences and Nutrition, Karolinska Institutet, Hälsovägen 7-9, Stockholm 14183, Sweden; mauro.damato{at}ki.se or Christopher Quince, School of Engineering, University of Glasgow, Rankine Building, Room 801, Glasgow G12 8LT, UK; christopher.quince{at}glasgow.ac.uk

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We read with interest the paper by Rehman et al 1 reporting the contribution of Nod2 genotype to the composition of gut microbiota in mice and Crohn's disease (CD) patients. This was followed by a similar description for another CD-predisposing gene, FUT2.2 To date, 163 CD- and ulcerative colitis-risk loci have been identified, and while most of the known causative genes are involved in immune functions and response to infections, their effects on the composition of the gut microbiota are mostly unknown. Studies like those mentioned above are therefore very important, since the relative abundance of specific enteric bacteria has been clearly shown to be of pathogenetic relevance in mouse models of colitis.3 By studying genotype–microbiota correlations in healthy individuals, key information could also be sought for devoid of potentially confounding effects from disease status and therapeutic treatment.

We studied the impact of 30 unequivocal CD-risk loci, each tagged by a single nucleotide polymorphism (SNP), on the mucosa-associated …

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Footnotes

  • CQ and EL contributed equally

  • Contributors MDA had the original idea, and designed the study together with LA and LE; ANA, NJT and LA collected and characterised the study subjects and acquired data; EL, ANA and LE performed sequencing of microbiota; MDA supervised genotyping; CQ, EL, ANA, AFA, JR and DG carried out statistical analyses; data analysis and interpretation was done by CQ and MDA, who drafted the manuscript with critical revision for important intellectual content from all other coauthors.

  • Funding Supported by funds from the Swedish Research Council (VR) to MDA and AFA, the Swedish Society of Medicine to LA, the EU project TORNADO to LE and JR and the Söderbergs Foundation to LE. CQ is funded through an EPSRC Career Acceleration Fellowship EP/H003851/1.

  • Competing interests None.

  • Ethics approval Karolinska Institutet, Stockholm, Sweden.

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

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