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• W4310784307 abstract "Particulate matter (PM2.5) is an environmental pollutant causing skin inflammatory diseases via epidermal barrier damage. However, the mechanism and related gene expression induced by PM2.5 remains unclear. Our aim was to determine the effect of PM2.5 on human skin tissue ex vivo, and elucidate the mechanism of T helper 17 cell-related inflammatory cytokine and skin barrier function. We verified the expression levels of gene in PM2.5-treated human skin tissue using Quantseq (3' mRNA-Seq), and Gene Ontology (GO) terms and protein-protein interaction (PPI) networks were performed. The PM2.5 treatment significantly enhanced the expression of Th 1, 2, 17 and 22 cell-related genes (cut-off value: │1.2 │ > fold change and p < 0.05). Most of all, Th17 cell-related genes are upregulated and those genes are associated with skin epidermal barrier function and Aryl hydrocarbon receptor (AhR), a xenobiotic receptor, pathway. In human keratinocyte cell lines, AhR-regulated genes (e.g. AhRR, CYP1A1, IL6 and IL36G), Th17 cell-related genes (e.g. IL17C) and epidermal barrier-related genes (e.g. SPRR2A and KRT71) are significantly increased after PM2.5. In the protein level, the secretion of IL-6 and IL-36G was increased in human skin tissue following PM2.5 treatment, and the expression of SPRR2A and KRT71 was significantly increased. PM2.5 exposure could ruin the skin epidermal barrier function via AhR- and Th17 cell-related inflammatory pathway." @default.
• W4310784307 created "2022-12-17" @default.
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• W4310784307 date "2022-12-27" @default.
• W4310784307 modified "2023-10-17" @default.
• W4310784307 title "Particulate matter 2.5 induces the skin barrier dysfunction and cutaneous inflammation via <scp>AhR</scp>‐ and T helper 17 cell‐related genes in human skin tissue as identified via transcriptome analysis" @default.
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• W4310784307 doi "https://doi.org/10.1111/exd.14724" @default.
• W4310784307 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/36471583" @default.
• W4310784307 hasPublicationYear "2022" @default.
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