Interleukin-25 Enhances Allergic Inflammation through p38MAPK and NF-κB Pathways in Mouse Models of Allergic Rhinitis

Abstract

Interleukin (IL)-25, a cytokine of IL-17 family, can activate p38 Mitogen-Activated Protein kinases(MAPK) and Nuclear Factor(NF)-κB pathways to propagate Th2 responses. The allergic rhinitis mouse model was established by stimulating BALB/c mouse with ovalbumin (OVA). Then we detected expression of IL-25 and downstream p38MAPK and NF-κB. The expression of IL-25, p38MAPK and NF-κB were detected in the OVA-induced allergic rhinitis mouse model. The allergic parameters, such as allergic symptoms, serum OVA-specific immunoglobulin E (IgE) levels and eosinophil infiltration in the nasal mucosa were compared between OVA group and control group. OVA-induced mice displayed significantly higher allergic responses compared with the saline control group. OVA induced mice demonstrated more allergic symptoms, higher serum OVA-specific IgE levels and eosinophil infiltrations. The increased expression of IL-25, p38MAPK and NF-κB immunoreactivity were detected in epidermal cells in the OVA group. The mRNA measurement of IL-25, p38MAPK and NF-κB showed the same result. IL-25 enhances the OVA-induced allergic rhinitis by activating p38MAPK and NF-κB pathways.

Keywords

• Allergic rhinitis
• Interleukin-25
• Mice
• NF-kappa B
• p38 Mitogen-Activated