Interleukin-18 and interleukin-18 receptor-α expression in allergic asthma

To the Editors: The inflammatory process in allergic asthma is initiated by T-helper (Th) type-2 cells, which produce a repertoire of cytokines, including interleukin (IL)-4, IL-5, IL-9 and IL-13, which are necessary for immunoglobulin (Ig)E production, airway eosinophilia and goblet cell hyperplasia [1]. IL-18 is another pro-inflammatory cytokine, initially described as interferon (IFN)-γ-inducing factor [2]. IL-18 can act as a cofactor for Th2 cell development and IgE production [3]. Recently, an IL-18 gene polymorphism was reported to be associated with asthma severity and higher serum IL-18 levels: the rs5744247 variant, which has higher transcriptional activity than the wildtype allele [4]. In addition, the IL-18 receptor (IL-18R) gene (on 2q21) has been identified as a candidate gene associated with increased susceptibility to asthma in children [5], and polymorphisms of the gene have been associated with allergic asthma and airway hyperresponsiveness (AHR) [6]. We have evaluated serum levels of IL-18 and the expression of IL-18Rα, as well as other Th2-associated cytokines, in stable allergic asthmatic subjects, compared with allergic nonasthmatic subjects and healthy controls. We studied 36 subjects, which included 15 allergic asthmatic subjects, 11 nonasthmatic allergic subjects and 10 healthy controls (table 1). All subjects underwent a methacholine inhalation challenge [7] and had skin-prick tests to a panel of 16 environmental allergens. Total IgE, and serum IL-18, IL-4, IL-10, IL-12, IL-13 and IFN-γ were measured using commercially available ELISA kits (Medical and Biological Laboratories Co., Nagoya, Japan; RD DRG International Inc., Mountainside, NJ, USA). The allergic subjects were studied outside …