Background: Interleukin-23 (IL-23) and IL-17 may be involved in the pathogenesis of allergic rhinitis (AR). However, a differentiation of the role of IL-23 and IL-17 has not been performed yet.
Objective: The aim of this study was therefore to investigate the immunomodulatory effects of IL-23 and IL-17, using a mouse model of AR.
Methods: Anti-IL-23p19 and anti-IL-17 Abs were administrated intranasally during rechallenge in ovalbumin (OVA)-induced AR in BALB/c mice. Immunomodulatory effects were evaluated by measuring nasal rubbing and sneezing occurrences, serum OVA-specific antibodies, Th2 responses (i.e. expression of IL-4, IL-5, IL-13 and IFN-γ genes in nasal mucosa, IL-4(+) CD4(+) T cells percentages in superficial cervical lymph nodes (LNs) and IL-4 production in LNs stimulated with OVA in vitro), and neutrophil, eosinophil and mast cell recruitment into the nasal mucosa.
Results: The effect of IL-17 antagonism was limited to attenuating the Th2 responses and neutrophil and eosinophil infiltration. In contrast, treatment with anti-IL-23p19 Abs markedly reduced nasal rubbing and sneezing events, Th2 responses, serum OVA-specific IgE and IgG1 levels, as well as mucosal neutrophil, eosinophil and mast cell infiltration.
Conclusion and clinical relevance: IL-17 and IL-23 may play a pathogenic role in an established AR mouse model; with a more pronounced contribution of IL-23 than IL-17.
Keywords: allergic rhinitis; immunomodulation; interleukin-17; interleukin-23; mouse model of AR.
© 2013 John Wiley & Sons Ltd.