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. 2025 Apr;155(4):1236-1249.e5.
doi: 10.1016/j.jaci.2024.10.034. Epub 2024 Nov 12.

Mesenchymal stem cell-derived small extracellular vesicles restored nasal barrier function in allergic rhinitis via miR-143-GSK3B in human nasal epithelial cells

Meiqian Xu  1 , Mei Ren  1 , Xinyin Zhang  1 , Wenxu Peng  1 , Hao Li  1 , Wenjing Liao  2 , Jianlei Xie  3 , Xiaowen Zhang  4
Affiliations

Mesenchymal stem cell-derived small extracellular vesicles restored nasal barrier function in allergic rhinitis via miR-143-GSK3B in human nasal epithelial cells

Meiqian Xu et al. J Allergy Clin Immunol. 2025 Apr.

Abstract

Background: The nasal epithelial barrier is the first line of defense against the deep entry of pathogens or aeroallergens and is more critical in allergic rhinitis (AR). Restoring epithelial barrier dysfunction might be a promising strategy for AR. Recent studies reported that mesenchymal stem cell-derived small extracellular vesicles (MSC-sEV) potentially inhibit the inflammation response and promote tissue regeneration. However, their effect on nasal epithelial cells remains unknown.

Objectives: This study sought to describe the therapeutic effect of MSC-sEV on AR, particularly focusing their effect on nasal epithelial cells and underlying molecular mechanisms.

Methods: We utilized an ovalbumin-induced mouse model to study AR. Both primary and immortalized human nasal epithelial cells (HNEpC) were used to further validate the therapeutic effects of MSC-sEV on epithelial cell function. Then we constructed microRNA (miR)-143 overexpressing and low-expressing HNEpC and MSC-sEV to elucidate molecular mechanisms. Transcriptome analysis was performed to identify the downstream pathways involved.

Results: MSC-sEV successfully maintained nasal barrier integrity in AR mouse model. The MSC-sEV therapeutic effect on the nasal barrier was substantiated in HNEpC. Mechanistically, miR-143 was a candidate mediator of the above effects. Subsequently, transfecting HNEpC with miR-143 partially mimicked the restoring effect of MSC-sEV. MSC-sEV overexpressing miR-143 exerted more therapeutic effects on tight junctions and barrier integrity. Moreover, miR-143 regulated the glycogen synthase kinase-3β (GSK3B) pathway.

Conclusions: Our results indicated that MSC-sEV mitigated AR and restored nasal epithelial barrier dysfunction through the miR-143-GSK3B axis, which suggested that MSC-sEV have the remarkable ability to treat AR.

Keywords: AR; MSC-sEV; epithelial barrier.

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Conflict of interest statement

Disclosure statement This study was supported by National Natural Science Foundation (82201251), National Clinical Key Specialty Construction Project (2021–2024), Guangzhou Medical Key Discipline Construction Project (2021–2023), Guangzhou202009030007, Zhongnanshan Medical Foundation of Guangdong Province ZNSA-2020013), Guangzhou Medical University Academic Innovation Ability Improvement Program (2022-2025), National Natural Science Foundation of China (grant no. 32101060), and State Key Laboratory of Respiratory Disease (grant no. SKLRD-Z-202218). Disclosure of potential conflict of interest: The authors declare that they have no relevant conflicts of interest.

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