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Human Molecular Genetics Advance Access published online on February 17, 2005
Human Molecular Genetics, doi:10.1093/hmg/ddi087
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© The Author 2005. Published by Oxford University Press. All rights reserved

Article

NOD1 variation, Immunoglobulin E, and asthma

Pirro Hysi 1, Michael Kabesch 2, Miriam F. Moffatt 1, Michaela Schedel 2, David Carr 2, Youming Zhang 1, Brenda Boardman 3, Erika von Mutius 2, Stephan K. Weiland 4, Wolfgang Leupold 5, Christian Fritzsch 6, Norman Klopp 7, A. William Musk 8, Alan James 8, Gabriel Nunez 9, Naohiro Inohara 10, and William O.C. Cookson 11*

1 Wellcome Trust Centre for Human Genetics, University of Oxford, UK
2 University Children's Hospital, Munich, Germany
3 Environmental Change Unit, University of Oxford, UK
4 Department of Epidemiology, University of Ulm, Ulm, Germany
5 University Children's Hospital Dresden, Germany
6 University Children's Hospital Leipzig, Germany
7 GSF Research Centre for Environment and Health, Neuherberg, Germany
8 Department of Respiratory Medicine, Sir Charles Gairdner Hospital, Perth, Western Australia
9 Department of Pathology, Univ of Michigan Med School, Ann Arbor, MI, USA
10 Comprehensive Cancer Center, Department of Pathology, Univ of Michigan Med School, Ann Arbor, MI, USA
11 Wellcome Trust Centre for Human Genetics, University of Oxford, Roosevelt Drive, Oxford OX3 7BN, UK

* To whom correspondence should be addressed.
William O.C. Cookson, E-mail: wocc{at}well.ox.ac.uk


  Abstract

Asthma is a familial inflammatory disease of the airways of the lung. Microbial exposures in childhood protect against asthma through unknown mechanisms. The innate immune system is able to identify microbial components through a variety of pattern-recognition receptors (PRRs). NOD1 is an intracellular PRR that initiates inflammation in response to bacterial diaminopimelic acid (iE-DAP). The NOD1 gene is on chromosome 7p14, in a region that has been genetically linked to asthma. We carried out a systematic search for polymorphism in the gene. We found an insertion-deletion polymorphism (ND1+32656) near the beginning of intron IX that accounted for approximately 7% of the variation in IgE in two panels of families (P<0.0005 in each). Allele*2 (the insertion) was associated with high IgE levels. The same allele was strongly associated with asthma in an independent study of 600 asthmatic children and 1194 super-normal controls (OR 6.3, 95%CI 1.4-28.3, dominant model). Differential binding of the two ND1+32656 alleles was observed to a protein from nuclei of the Calu 3 epithelial cell line. The deletion allele (ND1+32656*1) was found to be associated with Inflammatory Bowel Disease (IBD) in an accompanying study. The results indicate that intracellular recognition of specific bacterial products affects the presence of childhood asthma.


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