TLR2 Is Required for OVA-Induced Inflammatory Cells Infiltration, IgE, and Th2 Cytokines Production
In addition to lung histological changes, airway challenged with OVA induced a significant increase in total BALF cellularity in comparison with that of control mice (Figure 2A). Further morphologic assessments of differentially stained BALF samples revealed that the increase in cellularity was resulted from a significant influx of neutrophils, lymphocytes, monocytes and eosinophils (Figures 2B–E). However, in comparison with WT mice, the total number or composition of the BALF cellularity in TLR2−/− mice post OVA challenge was significantly decreased except for monocytes, which trended to increase but did not reach statistical significance (Figures 2A–E). Meanwhile, the level of OVA-specific IgE in TLR2−/− mice was significantly lower than that of WT mice (Figure 2F). Furthermore, significant increase in the levels of Th2-associated cytokines including IL-4 and IL-13 was observed in OVA-challenge WT mice (Figures 2E,F). Similarly, significant differences between WT and TLR2−/− mice were observed that TLR2 deficiency significantly decreased the levels of these two Th2-associated cytokines post OVA challenge (Figures 2G,H). Together, these data supported the role of TLR2 in the development of allergic airway inflammation in this OVA model.
Figure 2  TLR2 is required for OVA-induced inflammatory cells infiltration, IgE and Th2 cytokines production. (A) Total cell counts in the BALF of WT and TLR2−/− mice. (B–E) Differential cell counts in BALF of WT and TLR2−/− mice. (F) The level of OVA-specific IgE in serum. (G,H) Productions of IL-4 and IL-13 in BALF of WT and TLR2−/− mice were analyzed by ELISA. *p < 0.05, **p < 0.01, ***p < 0.001.