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.