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Background: Patients with aspirin‐exacerbated respiratory disease (AERD) are among the most challenging rhinologic patients to treat. AERD has a complex inflammatory milieu of lipid mediators and cytokines. In this study we evaluated cytokine differences in the complex AERD environment at the mucus, epithelial, and tissue levels. Methods: Samples were acquired at the time of sinus surgery from 21 patients (seven steroid‐treated, 14 untreated) with aspirin challenge‐confirmed AERD. Three methods (sponge adsorption, epithelial brushing, tissue biopsy) were used to acquire samples from the respective sinus sampling sites (mucus, polyp epithelium, and full‐thickness polyp) of each patient. We measured and compared 16 cytokine concentrations in AERD patients with or without prednisone treatment using the Luminex platform. Results: In most sampling sites, IL‐5, IL‐6, IL‐10, IL‐13, IL‐33, CCL20, and TNF‐α were detected at higher concentrations than IFN‐γ, IL‐1β, IL‐17A, IL‐4, IL‐22, IL‐17E/IL25, and GM‐CSF. Each sampling site had a different pattern of cytokine levels, and except for IL‐5 and IL‐25 there was no correlation among sampling methods for each cytokine tested. The most notable and significant decreases in cytokines from those treated with prednisone were observed in the epithelium for IL‐5, IL‐10, IL‐33, and IFN‐γ. Conclusions: In the epithelial samples, type 2‐associated cytokines IL‐5 and IL‐33, the anti‐inflammatory cytokine IL‐10, and IFN‐γ were lower in AERD patients treated with prednisone. This work serves as a basis to assess therapeutic‐induced mucosal cytokine responses in AERD and indicates that the site of cytokine measurement is an important consideration when assessing results. [ABSTRACT FROM AUTHOR]

This article discusses the long-term effects of aspirin desensitization on the inflammatory response in patients with aspirin-exacerbated respiratory disease (AERD). The study found that after long-term aspirin desensitization, there were significant increases in interferon-gamma (IFN-γ) and interleukin-10 (IL-10), suggesting a shift in the inflammatory response. These cytokines are associated with immune tolerance and may play a role in the mechanism of aspirin desensitization. However, the specific cells producing these cytokines and the role of lipid mediators in aspirin desensitization were not addressed in this study. Further research is needed to understand the cellular context and mechanisms associated with these cytokine shifts. [Extracted from the article]