Abstract
Background
Although Interleukin (IL)-17A has been suggested to play a role in corticosteroid hyporesponsiveness, whether IL-17A is able to affect the sensitivity of MUC5AC to intranasal corticosteroid treatment in patients with allergic rhinitis (AR) is unclear.
Methods
Twenty patients with moderate to severe AR were enrolled in this study and the expression of MUC5AC, IL-17A, and glucocorticoid receptor beta (GR beta) was detected using immunochemical staining and quantitative reverse transcription polymerase chain reaction (RT-PCR) before and after treatment with fluticasone propionate (FP) nasal spray for 4 weeks, respectively. In addition, the effects of FP on IL-13– and IL-17A–induced MUC5AC and GR beta were also evaluated in the primarily cultured human nasal epithelial cells (HNECs) in vitro.
Results
The increased MUC5AC expression was associated with IL-17A levels in AR, and IL-17A was found to affect the inhibition of MUC5AC by corticosteroid treatment. Both IL-13 and IL-17A significantly promoted MUC5AC mRNA expression in HNECs, and FP treatment was able to significantly inhibit MUC5AC mRNA expression in HNECs induced by IL-13 but not for that induced by IL-17A. Also, IL-17A but not IL-13 promoted GR beta mRNA expression in HNECs, which was not affected by administration of corticosteroid.
Conclusion
Our results suggest that the sensitivity of MUC5AC to topical corticosteroid is negatively associated with IL-17A in AR patients. This might help us to gain more insight into the pathophysiology and the pharmacotherapeutic mechanisms on AR treatment.
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