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Human Molecular Genetics Advance Access originally published online on March 24, 2005
Human Molecular Genetics 2005 14(10):1245-1250; doi:10.1093/hmg/ddi135
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© The Author 2005. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oupjournals.org

Association between a complex insertion/deletion polymorphism in NOD1 (CARD4) and susceptibility to inflammatory bowel disease

Dermot P.B. McGovern1,2,*, Pirro Hysi1, Tariq Ahmad2, David A. van Heel3, Miriam F. Moffatt1, Alisoun Carey4, William O.C. Cookson1 and Derek P. Jewell2

1The Wellcome Trust Centre for Human Genetics, University of Oxford, Roosevelt Drive, Headington, Oxford OX3 7BN, UK, 2Gastroenterology Unit, University of Oxford, Radcliffe Infirmary, Oxford, 3Imperial College, Hammersmith Campus, London, UK and 4Oxagen Ltd, Abingdon, Oxfordshire, UK

* To whom correspondence should be addressed. Tel: +44 1865 287651; Fax: +44 1865 287533; Email: dermot{at}well.ox.ac.uk

Received November 19, 2004; Revised March 11, 2005; Accepted March 21, 2005

The identification of the role of genetic variants within NOD2 (CARD15) in Crohn's disease and ulcerative colitis susceptibility highlight the role of the innate immune system in inflammatory bowel disease (IBD) pathogenesis. NOD1 (CARD4) is located on chromosome 7p14.3, in a region of known linkage to IBD and encodes an intracellular bacterial pathogen-associated molecular pattern receptor that is closely related to NOD2. We have identified strong association between haplotypes in the terminal exons of NOD1 and IBD (multi-allelic P=0.0000003) in a panel of 556 IBD trios. The deletion allele of a complex functional NOD1 indel polymorphism (ND1+32656*1) was significantly associated with early-onset IBD (P=0.0003) in unrelated cases and controls. ND1+32656*1 was also associated with extra-intestinal manifestations of IBD (P=0.04). These findings in two independent populations provide strong evidence for a role for NOD1 variants in IBD susceptibility and reinforce the role of the innate immune system in IBD pathogenesis.


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