TNF-α contributes to the development of allergic rhinitis in mice

Abstract

Background: Allergic rhinitis is an inflammation involving TH2-type cytokine production, with pathologic eosinophil infiltration in the nasal mucosa. Although TNF-α is thought to be a pro-inflammatory cytokine, the relationship between TNF-α and allergic rhinitis has not been clarified. Objectives: The role of TNF-α in a murine model of ovalbumin (OVA)-sensitized allergic rhinitis was investigated by using mice deficient in the gene encoding TNF-α (TNF-α-/- mice). Methods: Both wild-type (TNF-α+/+) and TNF-α-/- mice were sensitized with OVA by means of intraperitoneal injection. They were then challenged with intranasal OVA, and various allergic responses were assessed. Results: The production of OVA-specific IgE in the serum (P < .05) and the frequency of sneezes (P < .05) and nasal rubs (P < .05). Furthermore, the expression of both endothelial-leukocyte adhesion molecule 1 and vascular cell adhesion molecule 1 mRNA in the nasal mucosa was significantly suppressed (P < .05). Conclusion: TNF-α is necessary for antigen-specific IgE production and for the induction of TH2-type cytokines and chemokines. Furthermore, TNF-α might be important for the expression of adhesion molecules to recruit eosinophils to the allergic inflammatory site. We conclude that the lack of TNF-α inhibited the development of allergic rhinitis.