Interleukin 1βMediates the Pathogenesis of Nasal Mucosal Epithelial Barrier Dysfunction in Allergic Rhinitis

Background: The nasal mucosal epithelial barrier is the primary site of allergic rhinitis (AR). Interleukin-1(3 (IL-1(3), as a crucial factor in immune inflammation, not only plays a crucial role in hypersensitivity reactions but also affects the digestive mucosa and skin epithelial barrier. However, the role of IL-1(3 in the nasal mucosal epithelial barrier in AR has not been reported, and this study aimed to investigate the effect and possible mechanisms involved. Methods: Dermatophagoides pteronyssinus 1 was used as an allergen to construct an AR mouse model and stimulate human nasal mucosal epithelial cells (HNEpCs) and observe the expression changes of IL-1(3 and epithelial barrier indicators CLDN1 and OCLN in mouse nasal mucosa and HNEpCs. Then, the possible mechanisms of action were explored via exogenous IL-1(3 stimulation and pharmacological inhibition of IL-1(3 or its receptor interleukin-1 receptor type 1 (IL-1R1). Results: The results showed that Dermatophagoides pteronyssinus 1-primed mouse nasal mucosa or human HENpCs had increased expression of IL-1(3 and decreased CLDN1 and OCLN, and IL-1(3 could directly lead to reduced expression of epithelial barrier indexes in HNEpCs. In addition, inhibition of IL-1(3 or IL-1R1 can effectively alleviate the damage to the epithelial barrier. Conclusion: IL-1(3 has a destructive effect on the nasal mucosal epithelial barrier in AR, and inhibition of IL-1(3 or its receptor IL1R1 can effectively protect the nasal mucosal barrier. IL-1(3 is a potential target for the treatment of AR.