Amelioration of experimental allergic rhinitis with suppression of topical immune responses by lack of IL-27/WSX-1 signaling

Abstract

Allergic rhinitis is 1 of the most common atopic diseases with strong similarity to asthma. Interleukin (IL) 27 is an immunosuppressive cytokine, and lack of the IL-27 receptor (WSX-1) resulted in exacerbation of allergic airway hyperresponsiveness. To address the role of IL-27/WSX-1 in the rhinitis model compared with the asthma model. Wild-type or WSX-1(-l-) female mice were immunized intraperitoneally 4 times with ovalbumin adsorbed to aluminum potassium sulfate at a 1-week interval. The sensitized mice were then challenged for 14 days with ovalbumin intranasally from days 22 to 35. Clinical scores, serum antigen specific IgE levels, and cytokine production in the nasal lavage fluid were examined. Cytokine and chemokine expression in the cervical lymph nodes, nasopharynx-associated lymphoid tissues, and nasal mucosa was also examined. WSX-1(-l-) mice developed augmented immune responses in the serum (IgE production), cervical lymph nodes (cytokine and chemokine expression), and nasopharynx-associated lymphoid tissues (cytokine and chemokine expression), whereas local responses, such as clinical scores and nasal lavage fluid cytokine production, were reduced in WSX-1(-l-) mice. Expression of some chemokines was also reduced in the nasal mucosal tissues of WSX-1(-l-) mice. In contrast to the immunosuppressive role observed in the asthma model, IL-27/WSX-1 topically plays an exacerbating role in the pathogenesis of allergic rhinitis, presumably through differential expression of chemokines.