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The genetic basis of atopic asthma

Asthma is a respiratory disease characterized by recurrent respiratory symptoms, reversible variable airway obstruction, airway inflammation and increased airway responsiveness [1]. Atopy is a disorder involving immunoglobulin E (IgE) antibody responses to ubiquitous allergens, and is commonly associated with asthma. Because of its complex clinical phenotype, the genetic basis of asthma can be studied using intermediate or surrogate phenotypes that can be measured objectively, such as the presence of atopy or bronchial hyperresponsiveness (BHR), although these are not specific to asthma. Furthermore, despite the close relationship between atopy, bronchial hyperresponsiveness and asthma [2–4], they are not interchangeable: most asthmatics are atopic, but atopic subjects may not have bronchial hyperresponsiveness or asthma symptoms and subjects with bronchial hyperresponsiveness may not be atopic or asthmatic (see Fig. 1). The phenotype can be defined in several ways ranging from subjective measures (e.g. symptoms), objective measures (e.g. BHR or serum IgE level) or both. It is this lack of a clear definition of asthmatic phenotypes that presents the biggest problem when reviewing studies of the genetic basis of asthma and atopy, with multiple definitions of the same intermediate phenotype being used in different studies.