Association of the ADAM33 gene with asthma and bronchial hyperresponsiveness

Paul Van Eerdewegh, Randall D. Little, Josée Dupuis, Richard G. Del Mastro, Kathy Falls, Jason Simon, Dana Torrey, Sunil Pandit, Joyce McKenny, Karen Braunschweiger, Alison Walsh, Ziying Liu, Brooke Hayward, Colleen Folz, Susan P. Manning, Alicia Bawa, Lisa Saracino, Michelle Thackston, Youssef Benchekroun, Neva Capparell, Mei Wang, Ron Adair, Yun Feng, JoAnn Dubois, Michael G. FitzGerald, Hui Huang, René Gibson, Kristina M. Allen, Alex Pedan, Melvyn R. Danzig, Shelby P. Umland, Robert W. Egan, Francis M. Cuss, Steuart Rorke, Joanne B. Clough, John W. Holloway, Stephen T. Holgate and Tim P. Keith ()
Additional contact information
Paul Van Eerdewegh: Genome Therapeutics Corporation
Randall D. Little: Genome Therapeutics Corporation
Josée Dupuis: Genome Therapeutics Corporation
Richard G. Del Mastro: Genome Therapeutics Corporation
Kathy Falls: Genome Therapeutics Corporation
Jason Simon: Genome Therapeutics Corporation
Dana Torrey: Genome Therapeutics Corporation
Sunil Pandit: Genome Therapeutics Corporation
Joyce McKenny: Genome Therapeutics Corporation
Karen Braunschweiger: Genome Therapeutics Corporation
Alison Walsh: Genome Therapeutics Corporation
Ziying Liu: Genome Therapeutics Corporation
Brooke Hayward: Genome Therapeutics Corporation
Colleen Folz: Genome Therapeutics Corporation
Susan P. Manning: Genome Therapeutics Corporation
Alicia Bawa: Genome Therapeutics Corporation
Lisa Saracino: Genome Therapeutics Corporation
Michelle Thackston: Genome Therapeutics Corporation
Youssef Benchekroun: Genome Therapeutics Corporation
Neva Capparell: Genome Therapeutics Corporation
Mei Wang: Genome Therapeutics Corporation
Ron Adair: Genome Therapeutics Corporation
Yun Feng: Genome Therapeutics Corporation
JoAnn Dubois: Genome Therapeutics Corporation
Michael G. FitzGerald: Genome Therapeutics Corporation
Hui Huang: Genome Therapeutics Corporation
René Gibson: Genome Therapeutics Corporation
Kristina M. Allen: Genome Therapeutics Corporation
Alex Pedan: Genome Therapeutics Corporation
Melvyn R. Danzig: Schering-Plough Research Institute
Shelby P. Umland: Schering-Plough Research Institute
Robert W. Egan: Schering-Plough Research Institute
Francis M. Cuss: Schering-Plough Research Institute
Steuart Rorke: Respiratory, Cell and Molecular Biology, Infection, Inflammation and Repair Research Division, School of Medicine, University of Southampton, Southampton General Hospital
Joanne B. Clough: Respiratory, Cell and Molecular Biology, Infection, Inflammation and Repair Research Division, School of Medicine, University of Southampton, Southampton General Hospital
John W. Holloway: Respiratory, Cell and Molecular Biology, Infection, Inflammation and Repair Research Division, School of Medicine, University of Southampton, Southampton General Hospital
Stephen T. Holgate: Respiratory, Cell and Molecular Biology, Infection, Inflammation and Repair Research Division, School of Medicine, University of Southampton, Southampton General Hospital
Tim P. Keith: Genome Therapeutics Corporation

Nature, 2002, vol. 418, issue 6896, 426-430

Abstract: Abstract Asthma is a common respiratory disorder characterized by recurrent episodes of coughing, wheezing and breathlessness. Although environmental factors such as allergen exposure are risk factors in the development of asthma, both twin and family studies point to a strong genetic component1,2. To date, linkage studies have identified more than a dozen genomic regions linked to asthma3. In this study, we performed a genome-wide scan on 460 Caucasian families and identified a locus on chromosome 20p13 that was linked to asthma (log10 of the likelihood ratio (LOD), 2.94) and bronchial hyperresponsiveness (LOD, 3.93). A survey of 135 polymorphisms in 23 genes identified the ADAM33 gene4 as being significantly associated with asthma using case-control, transmission disequilibrium and haplotype analyses (P = 0.04–0.000003). ADAM proteins are membrane-anchored metalloproteases with diverse functions, which include the shedding of cell-surface proteins such as cytokines and cytokine receptors5. The identification and characterization of ADAM33, a putative asthma susceptibility gene identified by positional cloning in an outbred population, should provide insights into the pathogenesis and natural history of this common disease.

Date: 2002
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DOI: 10.1038/nature00878

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