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<p>TLR9/MyD88/NF-κB pathway is closely associated with inflammatory diseases; however, its role in the progression of psoriasis remains rarely reported. An imiquimod-induced psoriasis mouse model was conducted. The expression levels of TLR9/MyD88/NF-κB pathway related proteins were detected by immunofluorescence and Western blotting. Histopathology changes in skins were observed by hematoxylin-eosin and Masson staining assays. qRT-PCR was used to detect the mRNA expression of inflammatory cytokines (IL-17 and IL-23) and key downstream target genes of NF-κB (CXCL10, CCL20, and IL-8). Finally, the relationship between TLR9/MyD88/NF-κB pathway and psoriasis was investigated by inhibitor or lentiviral transfection. We found that TLR9/MyD88/NF-κB pathway-associated proteins were significantly up-regulated in skin lesion of mouse model. The use of TLR9/MyD88/NF-κB pathway-related inhibitors or lentiviral transfection remarkably attenuated skin lesions in mice with psoriasis. Overall, our study demonstrated that the activation of TLR9/MyD88/NF-κB pathway aggravates psoriatic lesion in imiquimod-induced psoriasis mouse model. These findings pointed out that this pathway may be a potential valuable target for treating psoriasis and would be helpful to the development and application of drugs.</p>

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TLR9/MyD88/NF-κB pathway aggravates skin lesions in an imiquimod-induced psoriasis mouse model

  • 期刊论文

  • 发表日期：

    2026年7月11日

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  • Zhihao Yuan,
  • Zhiliang Xu,
  • Shihui Tong,
  • Fangfang Liao,
  • Fan Hong,
  • Yousheng Mao,
  • Qiuhe Song

摘要

TLR9/MyD88/NF-κB pathway is closely associated with inflammatory diseases; however, its role in the progression of psoriasis remains rarely reported. An imiquimod-induced psoriasis mouse model was conducted. The expression levels of TLR9/MyD88/NF-κB pathway related proteins were detected by immunofluorescence and Western blotting. Histopathology changes in skins were observed by hematoxylin-eosin and Masson staining assays. qRT-PCR was used to detect the mRNA expression of inflammatory cytokines (IL-17 and IL-23) and key downstream target genes of NF-κB (CXCL10, CCL20, and IL-8). Finally, the relationship between TLR9/MyD88/NF-κB pathway and psoriasis was investigated by inhibitor or lentiviral transfection. We found that TLR9/MyD88/NF-κB pathway-associated proteins were significantly up-regulated in skin lesion of mouse model. The use of TLR9/MyD88/NF-κB pathway-related inhibitors or lentiviral transfection remarkably attenuated skin lesions in mice with psoriasis. Overall, our study demonstrated that the activation of TLR9/MyD88/NF-κB pathway aggravates psoriatic lesion in imiquimod-induced psoriasis mouse model. These findings pointed out that this pathway may be a potential valuable target for treating psoriasis and would be helpful to the development and application of drugs.