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Published on: March 2, 2016
Interleukin-25 Enhances Allergic Inflammation through p38MAPK and NF-κB Pathways in Mouse Models of Allergic Rhinitis
Zhipeng Li1, Hui Wang2, Lisi Liu3
1Department of Otorhinolaryngology Head and Neck Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China. lizhipeng-rose@hotmail.com.
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.
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