Role of Toll-like receptor 2/NF-κB signaling pathway in the pathogenesis of allergic rhinitis

We investigated the expression and role of the toll-like receptor 2 (TLR2)/nuclear factor (NF)-kappa B signaling pathway in the pathogenesis of allergic rhinitis (AR). One hundred rats were randomly divided into five groups: control (Group A), AR (Group B), AR + peptidoglycan (Group C), AR + peptidoglycan + pyrrolidine dithiocarbamate (PDTC; Group D), and AR + peptidoglycan + beclomethasone (Group E). Changes in nasal mucosa morphology, inflammatory cell infiltration, interleukin (IL)-12, IL-13, and immunoglobulin E (IgE) levels, TLR2 mRNA expression levels, and NF-kappa B protein expression levels were detected. Allergic injury was clearly observed in AR rat models. Rats stimulated with peptidoglycan demonstrated an increase in T helper 1 (Th1) cytokine IL-12 (interleukin-12) expression and a significant decrease in T helper 2 (Th2) cytokine IL-13 (interleukin-13) and IgE expression. Additionally, the quantity of neutrophils detected in Group C significantly increased in comparison to Group B; this was associated with enhanced TLR2 and NF-kappa B expression, indicating that the Th1/Th2 ratio changed after allergen stimulation, provoking cellular immunity. When the rats were injected with PDTC or beclomethasone, two inhibitors of NF-kappa B, the expression of NF-kappa B in Groups D and E was decreased compared to Group B. Increased expression of IL-12 and reduced expression of IL-13 and IgE were also detected; however, the mean neutrophil counts in groups D and E were significantly decreased in comparison to Group B, suggesting that lower expression of NF-kappa B inhibited excessive cellular immunity in nasal mucosa, and that allergic damage was alleviated accordingly. Our findings suggest that inhibition of the TLR2/NF-kappa B signaling pathway could correct the imbalance of Th1/Th2 cytokines in AR rats, which would provide a novel means to prevent and treat allergic diseases.