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Peer-reviewedCC BY-NC-NDEnvironment & health (Washington, D.C.)

IL-17 Signaling Pathway: A Potential Signaling Pathway Mediating Neuroinflammation Induced by PM2.5.

  • Natong Liu1
  • Zhongshuo Ma1
  • Xiao Sun1
  • Liyan Zhao1
  • Jie Zhang2
  • Nan Zhang3
  • Xue Liang1
  1. 1School of Public Health, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, Shandong 250117, China.
  2. 2Biomedical Sciences College & Shandong Medicinal Biotechnology Centre, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, Shandong 250117, China.
  3. 3Medical Science and Technology Innovation Center, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, Shandong 250117, China.
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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.

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Cite

BibTeXRIS
BibTeX
@article{liu2026il17,
  title = {{IL-17 Signaling Pathway: A Potential Signaling Pathway Mediating Neuroinflammation Induced by PM2.5.}},
  author = {Natong Liu and Zhongshuo Ma and Xiao Sun and Liyan Zhao and Jie Zhang and Nan Zhang and Xue Liang},
  journal = {Environment \& health (Washington, D.C.)},
  year = {2026},
  month = jun,
  doi = {10.1021/envhealth.6c00080},
  url = {https://europepmc.org/article/MED/42903623},
  note = {CC BY-NC-ND},
}
RIS
TY  - JOUR
TI  - IL-17 Signaling Pathway: A Potential Signaling Pathway Mediating Neuroinflammation Induced by PM2.5.
AU  - Natong Liu
AU  - Zhongshuo Ma
AU  - Xiao Sun
AU  - Liyan Zhao
AU  - Jie Zhang
AU  - Nan Zhang
AU  - Xue Liang
PY  - 2026
DA  - 2026/06/03
JO  - Environment & health (Washington, D.C.)
DO  - 10.1021/envhealth.6c00080
UR  - https://europepmc.org/article/MED/42903623
AB  - 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.
SN  - 2833-8278
ER  -