Journal of Otolaryngology and Ophthalmology of Shandong University ›› 2026, Vol. 40 ›› Issue (6): 10-21.

• Airway Allergic Diseases: From Mechanism to Practice • Previous Articles    

Nasal epithelial cell injury and fibroblast inflammatory phenotype activation induced by PM2.5 organic components

ZHOU Jiayao1,2,3, ZHU Ying1,2,3, HU Huilin4, LI Zhipeng1,2,3, LIN Hai1,2,3, TANG Ru1,2,3, MAO Song1,2,3, GU Yuelong1,2,3, ZHAO Yue4, ZHANG Weitian1,2,3   

  1. 1. Department of Otorhinolaryngology & Head and Neck Surgery , Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200233, China2. Institute of Otorhinolaryngology Head and Neck Surgery, Shanghai Jiao Tong University, Shanghai 200233, China3. Shanghai Key Laboratory of Sleep Disordered Breathing, Shanghai 200233, China4. School of Environmental Science and Engineering, Shanghai Jiao Tong University, Shanghai 200240, China
  • Published:2026-11-03

Abstract: Objective The present study was conducted with the objective of investigating the differential effects of organic compounds(OCs)within PM2.5 on human nasal epithelial cells(hNEs)and human nasal fibroblasts(hNFs), and elucidating the underlying molecular mechanisms. Methods PM2.5 samples were collected in Shanghai, and OCs were extracted using dichloromethane. Primary hNEs and hNFs were isolated in vitro and stimulated with different concentrations of OCs. The assessment of cell viability and toxicity wasconducted by means of thecell counting kit-8(CCK-8)and lactate dehydrogenase(LDH)assays. The employment of transcriptomic sequencing(RNA-seq)and bioinformatics analysis was undertaken for the identification of differentially expressed genes, the performance of functional enrichment analysis, and the construction of protein-protein interaction networks. The validation of the sequencing results was conducted through the utilisation of quantitative real-time PCR(RT-qPCR). Results The study demonstrated that OCs significantly inhibited the proliferation of hNEs and induced cytotoxicity in a concentration- and time-dependent manner. However, no effect was observed on the viability of hNFs. Subsequent to OC stimulation, the expression levels of CYP1A1 and CYP1B1 were observed to be elevated, while AHRR expression was reduced in hNEs. Concurrently, the expression of MT1 family genes was found to be upregulated, suggesting activation of the AHR-CYP pathway and oxidative stress damage. Conversely, in hNFs, OC stimulation led to an upregulation of inflammatory factors LIF, IL6, and its receptor IL6R, accompanied by a compensatory increase in AHRR expression. Conclusion The induction of hNEs injury and inflammatory phenotype of hNFs by OCs is attributable to differential regulation of AHRR. These two cell types have been shown to synergistically participate in the inflammatory and remodeling processes of chronic rhinosinusitis, thus providing a novel perspective on the pathogenesis of PM2.5-induced CRS.

Key words: Fine particulate matter, Organic components, Nasal epithelial cells, Nasal fibroblasts, Chronic rhinosinusitis

CLC Number: 

  • R765
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