Interleukin-17A-induced inflammation does not influence the development of nasal polyps in murine model

Nasal polyposis associated with chronic rhinosinusitis (CRS) is a chronic inflammatory disease that is characterized by infiltration of many inflammatory cells. Meanwhile, interleukin (IL)-17A is a well-known proinflammatory cytokine that induces both eosinophilic and neutrophilic inflammation. We investigated the role of IL-17A in the development of nasal polyps in the CRS murine model.

Eosinophilic CRS with nasal polyps was induced by using ovalbumin (OVA) and Staphylococcus aureus enterotoxin B (SEB) in wild-type BALB/c and IL-17A knockout (KO) mice. Histopathologic changes of the sinonasal cavity were evaluated using hematoxylin and eosin, Periodic acid-Schiff, Sirius red, Masson's trichrome, and immunohistochemistry. The levels of total and OVA-specific immunoglobulin Es (IgEs) in sera were measured using enzyme-linked immunosorbent assay. The expression levels of IL-4, IL-5, and interferon-γ (IFN-γ) in the nasal mucosa were assessed by quantitative real-time polymerase chain reaction.

Under the IL-17A deficiency, total and OVA-specific IgEs in sera were reduced significantly. Infiltration of both eosinophils and neutrophils into the nasal mucosa, subepithelial fibrosis, and goblet cell count also decreased significantly in IL-17A KO mice treated with both OVA and SEB compared with those in the wild-type counterpart. However, there were no significant differences in the number of polypoid lesions among groups. Meanwhile, IL-4 increased and IFN-γ decreased in the nasal mucosa in IL-17A KO mice treated with both OVA and SEB.

This study suggests that even though IL-17A plays an important role in both nasal inflammation and remodeling, it does not influence the development of nasal polypoid lesions.