TLR2 Is Required for OVA-Induced Murine Allergic Airway Inflammation
We first set out to confirm the role of TLR2 in murine allergic airway disease. WT and TLR2−/− mice were sensitized and challenged with OVA following the protocol showed in Figure 1A. Immunohistochemistry and western blot results showed that TLR2 protein expression was significantly increased in OVA-challenged WT mice in comparison with that of control mice (Figures 1B,C), and TLR2 was expressed on various types of cells, such as epithelial cells and leukocytes. Concomitantly, lung histology showed an increase in leukocyte recruitment to peribronchial and mucous cell metaplasia in OVA-challenged WT mice (Figures 1D–G). In sharp contrast, OVA-challenged TLR2−/− mice showed reductions in inflammatory cells recruitment (Figures 1D,F) and airway PAS+ cells (Figures 1E,G) in comparison with that of OVA-challenged WT mice.
Figure 1  TLR2 is required for OVA-induced murine allergic airway inflammation. (A) Protocol of establishing allergic airway inflammation, and comparison of resolution of WT and TLR2−/− mice. (B) The expression of TLR2 in lung tissue from vehicle and OVA-challenged mice was analyzed by immunohistochemistry. (C) The protein expression of TLR2 in OVA-challenged WT mice analyzed by western blot and quantification of the protein expression of TLR2. (D) Histological evaluation of the airway inflammation by staining lung sections with H&E, arrows indicates infiltrated leukocytes. (E) Histological examination of mucus production in the lung sections stained with PAS, arrow heads indicates goblet cells. (F) Quantitative analysis of airway inflammation. (G) Quantitative of mucus production. Scale bar: 50 μm. **p < 0.01, ***p < 0.001.