Figure 1
Itln KD mice are protected from AHR, airway inflammation, mucus production, and allergic response in the OVA asthma model. (a) Pulmonary resistance in response to different concentration of intravenous acetycholine in WT and Itln KD mice after sensitization and challenge with OVA or saline. n=6–8 mice per group. (b) H&E staining of representative lung sections. Original magnification, × 200. (c) Inflammatory scores of lung sections were calculated as described in Methods. (d) Counts for macrophages, eosinophils, lymphocytes and neutrophils in BAL fluids. n=6–8 mice per group. (e) Periodic acid-Schiff (PAS) staining for mucus in representative lung sections. Original magnification, × 200. (f) The numbers of PAS-staining-positive cells were counted in four random fields for each lung section at × 200 magnification. (g) Immunohistochemistry for Muc5ac in representative lung sections at × 200 magnification. (h) Muc5ac transcripts levels were determined by quantitative PCR. (i) Serum OVA-specific IgE in peripheral blood was determined by ELISA. n=6–8 mice per group. Data are mean±s.e.m. **P<0.01; ***P<0.001 vs. Itln KD mice challenged with OVA. Results are representative of three individual experiments.
