Inhalation Toxicology, Год журнала: 2025, Номер unknown, С. 1 - 16
Опубликована: Май 27, 2025
Increasing evidence suggests that exposure to fine particulate matter (PM2.5) is associated with an elevated risk of respiratory diseases. However, the precise mechanisms by which PM2.5 influences inflammatory processes in allergic rhinitis (AR) remain insufficiently understood. The STAT pathway has been identified as a critical mediator immune and responses, but its specific role modulating PM2.5-induced effects nasal mucosa AR remains unclear. This study aims investigate impact on response during AR. We analyzed mRNA expression profiles (GSE215411) from Gene Expression Omnibus (GEO) database human mucosa-derived fibroblasts. Differential analysis differential genes (DEGs), were visualized through hierarchical clustering radar plots. GO/KEGG enrichment Set Enrichment Analysis (GSEA) key pathways, focusing enrichment. Protein-protein interactions (PPIs) within using STRING Cytoscapedatabase, revealing cytokine signaling predominant functional pathways. An model, induced ovalbumin sensitization whole-body ambient exposure, was utilized assess activation mucosal tissue. A total 426 DEGs fibroblasts following emphasizing involvement. Validation mouse model confirmed allergens activate pathway, Th2 cytokines. significantly activates AR, amplifying Th2-related response.
Язык: Английский