Journal of Shandong University (Health Sciences) ›› 2023, Vol. 61 ›› Issue (9): 47-55.doi: 10.6040/j.issn.1671-7554.0.2023.0524

• Preclinical Medicine • Previous Articles     Next Articles

PM2.5 induces inflammatory response in nasal epithelial cells through TLR4/NF-κB pathway

YANG Xiaozhe1,2, ZHAO Yan1,2, QING Hui3, WANG Xiangdong1,2,3, ZHANG Luo1,2,3   

  1. 1. Department of Otolaryngology Head and Neck Surgery, Beijing Tongren Hospital, Capital Medical University, Key Laboratory of Otolaryngology Head and Neck Surgery(Capital Medical University), Ministry of Education, Beijing 100730, China;
    2. Beijing Institute of Otolaryngology, Beijing Laboratory of Allergic Diseases, Beijing Municipal Education Commission, Beijing Key Laboratory of Nasal Diseases, Beijing 100005, China;
    3. Department of Allergy, Beijing Tongren Hospital, Capital Medical University, Beijing 100730, China
  • Received:2023-06-17 Published:2023-10-10

Abstract: Objective To investigate the mechanism of TLR4/NF-κB signaling pathway in the inflammatory response of nasal mucosal epithelial cells induced by fine particulate matter(PM2.5). Methods After healthy human nasal epithelial cells(HNEpCs)were exposed to PM2.5, the RNA was extracted for transcriptome analysis by Illumina sequencer. The expressions of TLR4, NFKB1 and NFKB1A were detected with quantitative real-time PCR(qRT-PCR). Results PM2.5 caused cell toxicity and abnormal regulation of transcriptome of HNEpCs, and abnormal expressions of TLR4, NFKBIA and IL1B. KEGG pathway analysis indicated that TLR4/NF-κB pathway was significantly enriched. The qRT-PCR validation experiment revealed that after PM2.5 exposure, TLR4 was up-regulated while NFKB1 was down-regulated, and NFKBIA,which inhibited NF-κB, was significantly down-regulated, thus leading to abnormal regulation of the TLR4/NF-κB pathway. Conclusion The abnormal regulation of TLR4/NF-κB in HNEpCs may play a crucial role in the nasal mucosa inflammatory response induced by PM2.5 exposure.

Key words: Nasal epithelial cell line, Fine particulate matter, Exposure model, Abnormal regulation of gene, Quantitative red-time, Transcriptome analysis, Nasal mucosa inflammation

CLC Number: 

  • R765.25
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