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
  • 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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