The IL-17 Receptor IL-17RE Mediates Poly(inosinic-cytidylic) Acid-Induced Inflammation in a Mouse Model of Allergic Lung Inflammation

Introduction Interleukin 17 receptor E (IL-17RE) is specific to the epithelial cytokine interleukin-17C (IL-17C). Asthma exacerbation are frequently caused by viral infections. Polycytidylic acid (polyl : C) mimics viral infections through binding to TLR-3. We and others have shown that polyl : C induces the expression of IL-17C in respiratory epithelial cells.
Aim To investigate the function of IL-17RE in a mouse model of allergic lung inflammation.
Methods Wildetyp (WT) and IL-17RE deficient mice were sensitized and challenged with OVA to induce allergic lung inflammation. PolyI : C was applied intranasally. Levels of pulmonary cytokines and chemokines were analyzed 24 hours post polyI : C treatment.
Results There were no differences in the pulmonary concentrations of the cytokines CCL5, IL-5, and IL-13 and the chemokines MIP-2 and KC between WT and IL-17RE-/- mice in the absence of allergic lung inflammation 24 hours post polyI : C treatment. Treatment with polyI : C in the presence of allergic lung inflammation resulted in significantly increased concentrations of IL-15, IL-13, CCL5, MIP-2, and KC in WT mice compared with IL-17RE-/-mice.
Summary These results indicate that IL-17RE mediates virus-triggered lung inflammation in experiment asthma.