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Gut doi:10.1136/gutjnl-2012-304214
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The impact of Crohn's disease genes on healthy human gut microbiota: a pilot study

  1. Mauro D'Amato5
  1. 1School of Engineering, University of Glasgow, Glasgow, UK
  2. 2Science for Life Laboratory, Department of Microbiology Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden
  3. 3Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden
  4. 4Stress Research Institute, Stockholm University, Stockholm, Sweden
  5. 5Department of Biosciences and Nutrition, Karolinska Institutet, Stockholm, Sweden
  6. 6Department of Medicine, University of Newcastle, Callaghan, New South Wales, Australia
  7. 7Science 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
  • Received 26 November 2012
  • Revised 26 November 2012
  • Accepted 29 November 2012
  • Published Online First 7 January 2013

We read with interest the paper by Rehman et al1 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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