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Human Molecular Genetics Advance Access originally published online on February 17, 2005
Human Molecular Genetics 2005 14(7):935-941; doi:10.1093/hmg/ddi087
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© The Author 2005. Published by Oxford University Press. All rights reserved. For Permissions, please e-mail: journals.permissions{at}oupjournals.org

NOD1 variation, immunoglobulin E and asthma

Pirro Hysi1, Michael Kabesch3, Miriam F. Moffatt1, Michaela Schedel3, David Carr3, Youming Zhang1, Brenda Boardman2, Erika von Mutius3, Stephan K. Weiland4, Wolfgang Leupold5, Christian Fritzsch6, Norman Klopp7, A. William Musk8, Alan James8, Gabriel Nunez9, Naohiro Inohara9 and William O.C. Cookson1,*

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

* To whom correspondence should be addressed at: Wellcome Trust Centre for Human Genetics, University of Oxford, Roosevelt Drive, Oxford OX3 7BN, UK. Tel: +44 1865 287607; Fax: +44 1865 287578; Email: wocc{at}well.ox.ac.uk

Received November 19, 2004; Accepted February 11, 2005

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 ~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 [odds ratio (OR) 6.3; 95% confidence interval (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. In an accompanying study, the deletion allele (ND1+32656*1) was found to be associated with inflammatory bowel disease. The results indicate that intracellular recognition of specific bacterial products affects the presence of childhood asthma.


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