Abstract
Background: The role of the nasal epithelium in the induction of a proper cytokine response in normal subjects and subjects with allergic rhinitis is still not completely elucidated. Methodology: We aimed to compare nasal epithelial immune responses in allergic rhinitis patients of different ages compared to healthy volunteers. Primary nasal epithelial cells from 47 subjects (33 normal and 17 with allergic rhinitis) were collected and cultured. Their unstimulated supernatants were analysed for 21 cytokines and chemokines. Statistical analysis was performed with the R statistical software and the RStudio interface. Results: Differences of the spontaneous release of epithelial cytokines and chemokines were noticed between the two study groups. The levels of GMCSF, MIP1A, MIP1B, IL28A, TNFA, CCL5 were significantly lower in the allergic rhinitis group compared to healthy volunteers’ group, independent of age. Most differences were noticed in the younger allergic rhinitis group (0-12 years old). Conclusions: Despite the cross-sectional nature of the study and the limited number of subjects, allergic rhinitis appears to be associated with dysfunction of cytokine and chemokine spontaneous release from nasal epithelial cells which may represent an abnormal innate immunity maturation pattern.
Highlights
Despite the dramatic increase of allergic rhinitis (AR), affecting 20%-30% of the global population [1], and the intense study of the role of allergy and innate immunity underpinning its pathophysiology, there are still critical knowledge gaps [2]
The levels of GMCSF, MIP1A, MIP1B, IL28A, TNFA, CCL5 were significantly lower in the allergic rhinitis group compared to healthy volunteers’ group, independent of age
Most differences were noticed in the younger allergic rhinitis group (0-12 years old)
Summary
Despite the dramatic increase of allergic rhinitis (AR), affecting 20%-30% of the global population [1], and the intense study of the role of allergy and innate immunity underpinning its pathophysiology, there are still critical knowledge gaps [2]. It is well known that central to the inflammatory cascade in AR, is an immunoglobulin E (IgE)-dependent response to extrinsic protein antigens orchestrated by eosinophils, T cells, mast cells and basophils, which release several mediators such as chemokines and cytokines [3, 4]. These mediators are released locally and maintain a persistent inflammation of the nasal mucosa by attracting inflammatory cells and interfering with the mucosal barrier. The role of the nasal epithelium in the induction of a proper cytokine response in normal subjects and subjects with allergic rhinitis is still not completely elucidated
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