Abstract
Background and Purpose When house dust mite (HDM), a common allergen, comes into the mucosal membrane, it may stimulate innate immunity. However, the precise role of interleukin- (IL-) 25 in the development of HDM-induced nasal allergic inflammation is still unclear. Therefore, we investigated the role of IL-25 in allergic rhinitis (AR) patients sensitized to HDM. Methods To confirm the production of IL-25 in human nasal epithelial cells (HNECs), we stimulated HNECs. IL-25 expression in the nasal mucosa from control, non-AR (NAR) patients, and HDM-sensitized AR patients was assessed using immunohistochemistry, and quantitative reverse transcription PCR. Correlations between IL-25 and other inflammatory markers were explored. Results An in vitro study showed significantly elevated concentrations of IL-25 in the HNEC samples with highest doses of HDM. Nasal tissues from AR patients sensitized to HDM showed significantly higher IL-25 expression, compared to those from the control or NAR patients. Moreover, the expression of IL-25 in nasal tissues from AR patients sensitized to HDM was positively associated with Th2 markers, such as ECP and GATA3. Conclusions IL-25 expression increased with high-dose HDM stimulation and was related to Th2 markers. Therefore, IL-25 neutralization might offer a new strategy for treating patients with HDM-sensitized AR.
Highlights
Allergic rhinitis (AR) is a Th2 immune-mediated hypersensitivity in the nasal mucosa characterized by nasal obstruction, rhinorrhea, sneezing, and itching [1]
We stimulated the human nasal epithelial cells (HNECs) with various concentrations of house dust mite (HDM) (25, 50, 100, and 200 μg/mL)
In our in vitro study, we found that only the highest concentration of HDM (200 μg/mL) significantly increased IL-25 secretions (Figure 1)
Summary
Allergic rhinitis (AR) is a Th2 immune-mediated hypersensitivity in the nasal mucosa characterized by nasal obstruction, rhinorrhea, sneezing, and itching [1]. It is accompanied by an accumulation of eosinophils and mast cells in the nasal mucosa, as well as increased serum levels of antigen-specific IgE [2]. Recent studies have demonstrated that epithelial cell-derived cytokines, including thymic stromal lymphopoietin (TSLP), interleukin- (IL-) 25, and IL-33, are critical regulators of innate and adaptive immune responses associated with Th2 cytokine-mediated inflammation at nasal mucosal tissues [3,4,5]. IL-25 neutralization might offer a new strategy for treating patients with HDM-sensitized AR
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