Calpeptin may reverse glucocorticoid-resistance of allergic rhinitis associated with cigarette smoke exposure by down-regulating interferon regulatory factor 1

 In nasal mucosa samples collected from control patients and those with AR and smoking complicated with AR (Smoke+AR), eosinophils were counted. Serum levels of cytokines interleukin (IL)-4, IL-5, and tumor necrotic factor (TNF)-α were also measured. In addition, 25 rats were divided into the following groups (five rats per group): control, AR, Smoke+AR, AR treated with dexamethasone (DEX+AR), and smoke-exposed AR treated with dexamethasone (DEX+Smoke+AR). Allergic inflammatory reactions, changes in Type II T helper cells (Th2) /Type II intrinsic lymphocyte (ILC2), and expression of the glucocorticoid receptor (GR)-related proteins were detected. Furthermore, 25 rats were divided into the following groups (five rats per group): control, AR, Smoke+AR, DEX+Smoke+AR, and calpeptin-treated cigarette smoke-exposed AR (CP+Smoke+AR). The effect of calpeptin on allergic inflammatory reactions, changes in Th2/ILC2 cells and expression of the GR-related proteins in AR rats exposed to cigarette smoke was evaluated. RPMI-2650 cells were divided into four groups: control, cigarette smoke extract (CSE), CSE+DEX, and CSE+CP. Glucocorticoid sensitivity was evaluated based on IL-8 levels induced by TNF-a. The effect of calpeptin on IL-8 levels and expression of GR-related proteins was evaluated.