PM2.5 activates IL-17 signaling pathway in human nasal mucosa-derived fibroblasts

Fine particulate matter (PM2.5) represents a prevalent environmental pollutant in the atmosphere, capable of exerting deleterious effects on human health. Numerous studies have indicated a correlation between PM2.5 exposure and the development of chronic upper airway inflammatory diseases. The objective of this study was to investigate the impact of PM2.5 on the transcriptome of fibroblasts derived from nasal mucosa. Initially, nasal mucosa-derived fibroblasts were isolated, cultured, and subsequently stimulated with PM2.5 (100 μg/mL) or an equivalent volume of normal culture medium for a duration of 24 h. Following this, total RNA from these cells was extracted, purified, and subjected to sequencing using next-generation RNA sequencing technology. Differentially expressed genes (DEGs) were then identified and utilized for functional enrichment analysis. A protein–protein interaction (PPI) network of DEGs was constructed, and validation of key genes and proteins was carried out using quantitative real-time PCR and ELISA methods. Results revealed 426 DEGs, comprising 276 up-regulated genes and 150 down-regulated genes in nasal mucosa-derived fibroblasts treated with PM2.5 compared to control cells. Functional enrichment analysis indicated that DEGs were predominantly associated with inflammation-related pathways, including the IL-17 signaling pathway. In alignment with this, PPI analysis highlighted that hub genes were primarily involved in the regulation of the IL-17 signaling pathway. Subsequent validation through quantitative real-time PCR and ELISA confirmed significant alterations in the relative expressions of IL-17 signaling pathway-related genes and concentrations of IL-17 signaling pathway related proteins in nasal mucosa-derived fibroblasts treated with PM2.5 compared to control cells. In conclusion, PM2.5 intervention substantially altered the transcriptome of nasal mucosa-derived fibroblasts. Furthermore, PM2.5 has the potential to exacerbate the inflammatory responses of these fibroblasts by modulating the expression of key genes in the IL-17 signaling pathway.