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Am. J. Respir. Crit. Care Med., Volume 161, Number 6, June 2000, 1836-1843

Independent Inheritance of Serum Immunoglobulin E Concentrations and Airway Responsiveness

LYLE J. PALMER, PAUL R. BURTON, JENNIE A. FAUX, ALAN L. JAMES, A. WILLIAM MUSK, and WILLIAM O. C. M. COOKSON

Department of Epidemiology and Biostatistics, Case Western Reserve University, Cleveland, Ohio; Genetic Epidemiology Unit, Department of Epidemiology and Public Health, University of Leicester, Leicester; Nuffield Department of Clinical Medicine, John Radcliffe Hospital, Oxford, United Kingdom; Department of Pulmonary Physiology, University Department of Medicine, and Department of Respiratory Medicine, Sir Charles Gairdner Hospital, and Genetic Epidemiology Unit, Division of Population Sciences, TVW Telethon Institute for Child Health Research, Perth, Australia

Elevated serum Immunoglobulin E (IgE) levels and increased airway responsiveness (AR) are correlated traits that are characteristic of asthma. It is not known to what extent these traits arise from distinct or shared genetic determinants. We investigated the genetic and environmental components of variance of serum total and specific IgE levels and AR in an Australian population-based sample of 232 Caucasian nuclear families. The inter-relationships of the genetic determinants of these traits were also investigated. Loge total serum IgE levels had a narrow-sense heritability (h2N) of 47.3% (SE = 10.0%). Specific serum IgE levels against house dust mite and timothy grass, measured as a RAST Index, ad a h2N of 33.8% (SE = 7.3%). AR, quantified by the loge dose-response slope to methacholine (DRS), had a h2N of 30.0% (SE = 12.3%). Extended modeling demonstrated an approximate 70% overlap in the genetic determinants of total and specific serum IgE levels. The genetic determinants of serum IgE levels and AR exhibited less than 30% sharing. These data are consistent with the existence of multiple genetic determinants of the pathophysiologic traits associated with asthma, and suggest that AR is genetically distinct from atopy. These results have implications for gene discovery programs.




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