Abstract: Objective　To experimentally investigate a potential mechanism of the TLR-NF-κB signaling pathway in the pathogenesis of allergic rhinitis (AR), and the role of NF-κB in eosinophil aggregation.　Methods　A total of 50 rats were randomly divided into five groups with A (control group), B (AR group), C (group of AR+PGN), D (group of AR+PGN+Pam3CSK4), and E (group of AR +PGN+BEL). AR model was established with ovalbumin. Hematoxylin and eosin (H&E) staining was used to detect the morphologic change of nasal mucosa and count the number of infiltrated inflammatory cell. The contents of IFN-γ, IL-4, MBP and IgE in nasal cleanser were detected by ELISA. Expression of NF-κB and TLR2 was measured by Real-Time polymerase chain reaction (PCR) and Western blot.　Results　Obvious allergic injury was observed in AR rats (B group). The number of infiltrated eosinophils in nasal mucosa in group B was higher than in other groups. The expressions of IL-4, MBP and IgE in group B were higher than in group A (P＜0.05). Neutrophil infiltration was predominant in nasal mucosa of group C, and the expression of IFN-γ, TLR2 and NF-κB was higher in group B (P＜0.05). Inflammatory cell infiltration, IL-4, MBP and IgE expression in group D and E were lower than in group B (P＜0.05).　Conclusions　Regulating the expression of TLR-NF-κB pathway and inhibiting the over-expression of NF-κB is beneficial to regulating the aggregation of eosinophils in the pathogenesis of allergic rhinitis.

Key words:  , NF-κB, 　 Toll-like receptor, 　 PGN, 　Eosinophils, 　Allergic rhinitis