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Letter
Paneth cell marker CD24 in NOD2 knockout organoids and in inflammatory bowel disease (IBD)
  1. Johan Van Limbergen1,2,
  2. Kaoru Geddes3,
  3. Paul Henderson2,
  4. Richard K Russell4,
  5. Hazel E Drummond5,
  6. Jack Satsangi5,
  7. Anne M Griffiths6,
  8. Dana J Philpott3,
  9. David C Wilson2
  1. 1Division of Gastroenterology and Nutrition, Department of Pediatrics, IBD Centre, Dalhousie University, Halifax, Nova Scotia, Canada
  2. 2Department of Child Life and Health, University of Edinburgh, Edinburgh, UK
  3. 3Department of Immunology, University of Toronto, Toronto, Ontario, Canada
  4. 4Department of Paediatric Gastroenterology, Yorkhill Hospital, Glasgow, UK
  5. 5Gastrointestinal Unit, University of Edinburgh, Edinburgh, UK
  6. 6Division of Paediatric Gastroenterology, Hospital for Sick Children, Toronto, Ontario, Canada
  1. Correspondence to  Dr Johan Van Limbergen, IBD Centre, Division of Gastroenterology & Nutrition, Department of Paediatrics, Dalhousie University, IWK Health Centre, 5850 University Avenue, Halifax, Nova Scotia, B3K 6R8, Canada; johanvanlimbergen{at}hotmail.com

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We read with great interest the article by Shanahan et al1 describing the roles of environmental conditions, notably co-housing with wild type (WT) littermates, and mouse genetic background in nucleotide-binding oligomerisation domain-containing protein 2 (NOD2)-dependent production of anti-microbial peptides in the mouse intestine. These authors demonstrate that expression, translation and anti-microbial activity of α-defensins are independent of NOD2.1 Robertson et al2 recently confirmed that housing conditions rather than NOD2 status influenced intestinal microbiota composition. Shanahan et al address the question whether an increase in the number of Paneth cells could compensate for a NOD2-dependent reduction in the level of defensin production in Paneth cells. Using a combination of hematoxylin and eosin staining (to assess crypt numbers), immunohistochemistry (using anti-lyzozyme staining) and flow cytometry (sorting for expression of lyzozyme and lack of expression of CD45—a haematopoietic cell marker) of the entire ilea of WT and NOD2-deficient mice showed NOD2 status did not influence Paneth cell numbers.1

CD24, a heavily glycosylated protein marker of intestinal crypt stem cells and Paneth cells, is upregulated in inflammatory bowel disease (IBD).3 ,4 Sato et al3 demonstrated that the combination of CD24hi and …

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Footnotes

  • Correction notice This article has been corrected since it was published Online First. The Funding statement has been amended.

  • Acknowledgements The authors would like to thank Dr S Middendorp, Prof E Nieuwenhuis and Prof H Clevers (Utrecht, the Netherlands) for their help and advice in setting up the intestinal organoid cultures.

  • Contributors JVL: study design, performed experiments, wrote manuscript. KG: study design, performed experiments, manuscript preparation. PH: genotyping, data analysis, manuscript preparation. RKR: patient and data collection, manuscript preparation. HED: patient and data collection, genotyping quality control, data analysis. JS: patient and data collection, study design, manuscript review. AMG: supervisor of experiments, study design, manuscript preparation. DJP: study design, supervisor of experiments, manuscript preparation. DCW: study design, genotyping, patient and data collection, manuscript preparation.

  • Funding JVL was supported by a Canadian Institutes for Health Research (CIHR)/Canadian Association of Gastroenterology Fellowship (234622), the University of Toronto Edward Christie Stevens Fellowship, Nellie L Farthing Fellowship, the William S Fenwick Fellowship, the Chisholm Memorial Fellowship, the Miriam Neveren Memorial Award and the Joseph M West Family Memorial Fund, and was the holder of the 2011 CIHR Bisby Fellowship. DP is a Howard Hughes International Scholar and is supported by the CIHR and Canadian Crohn's and Colitis Foundation (CCFC). PH was supported by a Medical Research Council project grant for PICTS to DW (G0800675), by Schering-Plough and the GI/Nutrition Research Fund, Child Life and Health, University of Edinburgh. RKR is supported by a NHS Research Scotland career fellowship award.

  • Competing interests None.

  • Ethics approval COREC.

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

  • Data sharing statement CD24 genotyping: only female patients and controls were analysed due to pseudogene on the Y chromosome.

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