Journal of Capital Medical University ›› 2026, Vol. 47 ›› Issue (4): 692-699.doi: 10.3969/j.issn.1006-7795.2026.04.009

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Fine particulate matter induces epithelial-mesenchymal transition in chronic rhinosinusitis with nasal polyps via the C3a/C3aR axis

Liang Shuang1,2, Yan Bing1,2,Li Ying 1,2,Wang Chengshuo1,2, Zhang Luo 1,2,3*   

  1. 1.Department of Otolaryngology Head and Neck Surgery, Beijing Tongren Hospital, Capital Medical University, Key Laboratory of Otorhinolaryngology Head and Neck Surgery (Capital Medical University), Ministry of Education, Beijing 100730, China; 2.Beijing Laboratory of Allergic Diseases, Beijing Municipal Education Commission and Beijing Key Laboratory of New Medicine and Diagnostic Technology Research for Nasal Disease, Beijing Institute of Otolaryngology, Beijing 100005, China；, China; 3.Department of Allergy, Beijing Tongren Hospital, Capital Medical University, Beijing 100730, China
  • Received:2026-04-08 Revised:2026-05-05 Online:2026-08-21 Published:2026-07-26
  • Supported by:
    This work was supported by grants from the National Key R&D Program of China (2023YFC2410200), National Natural Science Foundation of China （82471135，82401325，82025010), Special Funds for the Construction of High-level Public Health Technical Talents (Backbone of Academic Research-03-03).

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Abstract: Objective  To investigate the role of the complement C3a/C3aR axis in PM2.5-induced epithelial-mesenchymal transition (EMT) in chronic rihinosinusitis with nasal polyps (CRSwNP).Methods  The expression levels of the epithelial marker  E-cadherin and mesenchymal marker vimentin were detected by immunofluorescence staining in 50 μg/mL PM2.5-treated human primary nasal epithelial cells (HPNECs) from patients with CRSwNP. Public datasets (GSE220165 and GSE36830) were obtained to analyzed the expression of cadherin 1 and VIM, and Spearman' correlation analysis between the complement component 3a receptor (C3aR) and EMT-related molecules ［cadherin 1, VIM, zinc finger E-box binding homeobox 2 (ZEB2), and matrix metallopeptidase 9 (MMP9)］ were performed. Protein levels of C3a and C3aR in PM2.5-treated HPNECs were analyzed by Western blotting. EMT markers were examined in HPNECs after C3aR antagonist (C3aRA) treatment using immunofluorescence and Western blotting assays.Results  PM2.5 downregulated cadherin 1 and upregulated vimentin expression in HPNECs, in agreement with previously published transcriptomic data (GSE220165).  PM2.5 increased both C3a and its receptor C3aR levels in HPNECs. C3aR expression positively correlated with the EMT-related molecules ZEB2 (r=0.497, P=0.014 4) and MMP9 (r=0.409, P=0.048). Although its correlation with VIM exhibited a positive trend, it did not reach statistical significance (r=0.377, P=0.069 9). Blocking the C3a/C3aR axis with C3aRA partially alleviated PM2.5-induced downregulation of E-cadherin and upregulation of vimentin, ZEB2, and MMP9 in HPNECs.Conclusion  PM2.5 could induce EMT via activation of the C3a/C3aR axis in CRSwNP.

Key words: fine particulate matter (PM2.5), chronic rhinosinusitis with nasal polyps (CRSwNP), human primary nasal epithelial cells, complement component 3, complement component 3a receptor antagonist, epithelial-mesenchymal transition

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