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<p>Allergic conjunctivitis (AC) is an IgE-mediated type I hypersensitivity disorder characterized by conjunctival hyperemia, itching, and increased tear secretions. This study aims to investigate the mechanism of FOXP3 in the inflammatory activation of human conjunctival epithelial cells (HConEpiCs) in AC. Serum samples were collected from AC patients and healthy volunteers for correlation analysis of FOXP3 with inflammatory cytokines (IL-6/IL-8/TNF-α/CRP) and immunoglobulins (IgG/IgA/IgE). FOXP3, KAT5, and PDCD4 expression were measured by RT-qPCR, followed by Pearson correlation analysis. HConEpiCs were used to establish an AC cell model, followed by assessment of cell viability and inflammatory cytokines (IL-6/IL-8/TNF-α/IL-10/IL-4). The binding of FOXP3 to the KAT5 promoter and KAT5 and H3K27ac enrichment on the PDCD4 promoter were detected. FOXP3 expression was downregulated in AC patient, while KAT5 and PDCD4 were upregulated. FOXP3 negatively correlated with IL-6, IL-8, TNF-α, C-reactive protein, serum IgG, IgA, IgE, and eosinophil ratio. In histamine-stimulated HConEpiCs, FOXP3 overexpression inhibited inflammation. Mechanistically, FOXP3 bound to the KAT5 promoter to inhibit KAT5 expression, reduced KAT5 and H3K27ac enrichment on the PDCD4 promoter, and downregulated PDCD4 expression. KAT5 or PDCD4 overexpression reversed FOXP3-mediated inhibition of HConEpiC inflammatory activation. In conclusion, FOXP3 overexpression attenuates inflammatory activation of HConEpiCs by inhibiting KAT5 expression and reducing KAT5/H3K27ac-mediated PDCD4 transcription.</p>

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FOXP3 inhibits inflammatory activation of conjunctival epithelial cells in allergic conjunctivitis via the KAT5/PDCD4 axis

  • 期刊论文

  • 发表日期：

    2025年9月17日

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  • Zifeng Deng

摘要

Allergic conjunctivitis (AC) is an IgE-mediated type I hypersensitivity disorder characterized by conjunctival hyperemia, itching, and increased tear secretions. This study aims to investigate the mechanism of FOXP3 in the inflammatory activation of human conjunctival epithelial cells (HConEpiCs) in AC. Serum samples were collected from AC patients and healthy volunteers for correlation analysis of FOXP3 with inflammatory cytokines (IL-6/IL-8/TNF-α/CRP) and immunoglobulins (IgG/IgA/IgE). FOXP3, KAT5, and PDCD4 expression were measured by RT-qPCR, followed by Pearson correlation analysis. HConEpiCs were used to establish an AC cell model, followed by assessment of cell viability and inflammatory cytokines (IL-6/IL-8/TNF-α/IL-10/IL-4). The binding of FOXP3 to the KAT5 promoter and KAT5 and H3K27ac enrichment on the PDCD4 promoter were detected. FOXP3 expression was downregulated in AC patient, while KAT5 and PDCD4 were upregulated. FOXP3 negatively correlated with IL-6, IL-8, TNF-α, C-reactive protein, serum IgG, IgA, IgE, and eosinophil ratio. In histamine-stimulated HConEpiCs, FOXP3 overexpression inhibited inflammation. Mechanistically, FOXP3 bound to the KAT5 promoter to inhibit KAT5 expression, reduced KAT5 and H3K27ac enrichment on the PDCD4 promoter, and downregulated PDCD4 expression. KAT5 or PDCD4 overexpression reversed FOXP3-mediated inhibition of HConEpiC inflammatory activation. In conclusion, FOXP3 overexpression attenuates inflammatory activation of HConEpiCs by inhibiting KAT5 expression and reducing KAT5/H3K27ac-mediated PDCD4 transcription.