PM2.5 aggravates AR and promotes AR nasal mucosa inflammation. The influence of PM2.5 inhalation exposure on miRNA expression profiles and function in the nasal mucosa of AR rats was investigated.

Female Sprague Dawley rats were distributed randomly to 2 groups: AR model PM2.5 exposure group and AR model PM2.5-unexposed control group. The rats of the ARE group were made to inhale PM2.5 at a concentration of 200 µg/m3, 3 h/day, for 30 days.

Numerous target genes of differentially expressed miRNAs were functionally enriched in high-affinity immunoglobulin E receptor signaling, ErbB signaling, mucin O-glycans biosynthesis, transforming growth factor β signaling, mitogen-activated protein kinase signal transduction, phosphatidylinositol signaling, mucopolysaccharide biosynthesis, mammalian target of rapamycin signaling, T cell receptor signaling, Wnt signaling, chemokine signal transduction, and natural killer cell-mediated cytotoxicity pathways.

The study concluded that PM2.5 causes significant changes in miRNA expression in the nasal mucosa of AR rats. miRNA plays an essential role in regulating PM2.5 effects in AR rat biological behavior and mucosal inflammation. This study provides a theoretical basis for preventing and treating AR from the environmental pollution on the gene regulation mechanism.