BACKGROUND The interleukin 17 receptor E (IL-17RE) is specific for the epithelial cytokine interleukin-17C (IL-17C). Asthma exacerbations are frequently caused by viral infections . Polyinosinic: polycytidylic acid (pIC) mimics viral infections through binding to pattern recognition receptors (e.g . TLR-3). We and others have shown that pIC induces the expression of IL-17C in airway epithelial cells . Using different mouse models, we aimed to investigate the function of IL-17RE in the development of experimental allergic asthma and acute exacerbation thereof .
METHODS Wild-type (WT) and IL-17RE deficient (Il-17re) mice were sensitized and challenged with OVA to induce allergic airway inflammation . pIC or PBS were applied intranasally when allergic airway inflammation had been established . Pulmonary expression of inflammatory mediators, numbers of inflammatory cells, and airway hyperresponsiveness (AHR) were analyzed .
RESULTS Ablation of IL-17RE did not affect the development of OVA-induced allergic airway inflammation and AHR . pIC induced inflammation independent of IL-17RE in the absence of allergic airway inflammation . Treatment of mice with pIC exacerbated pulmonary inflammation in sensitized and OVA-challenged mice in an IL-17RE-dependent manner . The pIC-induced expression of cytokines (e.g . keratinocyte-derived chemokine (KC), granulocyte-colony stimulating factor (G-CSF) ) and recruitment of neutrophils were decreased in Il-17re mice . pIC-exacerbated AHR was partially decreased in Il-17re mice .
CONCLUSIONS Our results indicate that IL-17RE mediates virus-triggered exacerbations but does not have a function in the development of allergic lung disease.