To the Editors:
Asthma is a multifactorial disease. Although a number of host and environmental risk factors have been identified in the past decades, these cannot fully explain the prevalence of asthma. Previous studies have shown that psychosocial stress confers a risk for the development of asthma [1].
Stress activates the hypothalamus–pituitary–adrenal (HPA) axis, which leads to secretion of cortisol. Cortisol in turn influences the activity of many systems in the human body and shifts, among others, the T-helper type (Th1/Th2) balance of the peripheral blood mononuclear cells towards a predominantly type 2 response. Cortisol binds to the high affinity mineralocorticoid receptor (NR3C2) and the low affinity glucocorticoid receptor (NR3C1). Single nucleotide polymorphisms (SNPs) in these receptors have been associated with basal cortisol and cortisol responses to stress [2]. So far, two studies have found an association between SNPs inNR3C1(i.e.rs6195, rs41423247) and asthma development [3,4]. However, these results have not been replicated in other populations so far. Additionally, it is unknown whether other functional or tagging SNPs in theNR3C1are associated with asthma development. In addition, SNPs …