2. Academic Validation
  3. Interleukin 1β Mediates the Pathogenesis of Nasal Mucosal Epithelial Barrier Dysfunction in Allergic Rhinitis

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

  • J Inflamm Res. 2024 Nov 19:17:9071-9085. doi: 10.2147/JIR.S488340.
Hanrui Wang # 1 2 3 4,  Xiaoyu Song # 1 2 3 4,  Yao Wang 1 2 3 4,  Ting Yang 1 2 3 4,  Wanchen Liu 1 2 3 4,  Yakui Mou # 1 2 3 4,  Chao Ren 1 2 3 4 5,  Xicheng Song 1 2 3 4
Affiliations

Affiliations

  • 1 Department of Otorhinolaryngology, Head and Neck Surgery, Yantai Yuhuangding Hospital, Qingdao University, Yantai, People's Republic of China.
  • 2 Shandong Provincial Key Laboratory of Neuroimmune Interaction and Regulation, Yantai Yuhuangding Hospital, Yantai, People's Republic of China.
  • 3 Shandong Provincial Clinical Research Center for Otorhinolaryngologic Diseases, Yantai Yuhuangding Hospital, Yantai, People's Republic of China.
  • 4 Yantai Key Laboratory of Otorhinolaryngologic Diseases, Yantai Yuhuangding Hospital, Qingdao University, Yantai, People's Republic of China.
  • 5 Department of Neurology, Yantai Yuhuangding Hospital, Qingdao University, Yantai, People's Republic of China.
  • # Contributed equally.
PMID: 39588138 DOI: 10.2147/JIR.S488340
Abstract

Background: The nasal mucosal epithelial barrier is the primary site of allergic rhinitis (AR). Interleukin-1β (IL-1β), 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-1β 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-1β and epithelial barrier indicators CLDN1 and OCLN in mouse nasal mucosa and HNEpCs. Then, the possible mechanisms of action were explored via exogenous IL-1β stimulation and pharmacological inhibition of IL-1β 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-1β and decreased CLDN1 and OCLN, and IL-1β could directly lead to reduced expression of epithelial barrier indexes in HNEpCs. In addition, inhibition of IL-1β or IL-1R1 can effectively alleviate the damage to the epithelial barrier.

Conclusion: IL-1β has a destructive effect on the nasal mucosal epithelial barrier in AR, and inhibition of IL-1β or its receptor IL-1R1 can effectively protect the nasal mucosal barrier. IL-1β is a potential target for the treatment of AR.

Keywords

DerP1; allergic rhinitis; epithelial barrier; interleukin-1β; nasal mucous membrane.

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