IL-17信号通路：PM2.5诱导神经炎症的潜在信号通路

Abstract

Particulate Matter 2.5 (PM2.5) in the atmosphere can invade the central nervous system (CNS) and induce neurotoxicity, yet the mechanism is not well understood. In this study, the viability of microglia was significantly reduced by PM2.5, and the alteration of several inflammatory factors indicated an inflammatory response in BV2 cells caused by PM2.5. Differentially expressed genes (DEGs) were then screened by a microarray assay. These DEGs were mainly enriched in terms associated with inflammatory reactions through Gene Ontology (GO) annotation. Additionally, the Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis indicated that these DEGs were primarily enriched in IL-17 along with its downstream NF-κB and MAPK signaling pathways. Furthermore, the adverse impacts of PM2.5 exposure were effectively alleviated by the IL-17 signaling pathway inhibitor aIL17A, including improvements in the behavioral barrier, suppression of IL-17 activation and its downstream NF-κB and MAPK signaling pathways, reduced excessive secretion of inflammation cytokines, and decreased microglial activation. Combining all these results, PM2.5 was found to activate IL-17 along with its downstream NF-κB and MAPK signaling pathways, triggering microglial activation and neuroinflammation, ultimately leading to neurobehavioral impairments. Overall, the IL-17 signaling pathway may be a potential therapeutic target for PM2.5-induced neurotoxicity, which will contribute to related research in the future.