Background and Aims Psoriasis is a relatively common autoimmune inflammatory skin disease with a chronic etiology. Since psoriasis is still incurable, it is necessary to identify the molecular mechanisms of psoriasis. The present study was designed to detect novel biomarkers and pathways associated with psoriasis incidence, and provide new insights into treatment of psoriasis. Methods and Results Differentially expressed genes (DEGs) associated with psoriasis in the Gene Expression Omnibus (GEO) database were identified, and their functional roles and interactions were then annotated and evaluated through GO, KEGG, and gene set variation (GSVA) analyses. In total 197 psoriasis-related DEGs were identified and found to primarily be associated with the NOD-like receptor, IL-17, and cytokine-cytokine receptor interaction signalling pathways. GSVA revealed significant differences between normal and lesional groups (P < 0.05), while PPI network analyses identified CXCL10 as the hub gene with the highest degree value, whereas IRF7, IFIT3, OAS1, GBP1, and ISG15 were promising candidate genes for the therapeutic treatment of psoriasis. Conclusion The findings of the present integrated bioinformatics may enhance our understanding of the molecular events occurring in psoriasis, and these candidate genes and pathways together may prove to be therapeutic targets for psoriasis.
Uveitis is considered a relatively rare but serious ocular complication of psoriasis. We report the first successful treatment of severe noninfectious uveitis with secukinumab in a 70-year-old woman with erythrodermic psoriasis and psoriatic arthritis. Anti-tumor necrosis factor (TNF) agents were administered for 5 years for the treatment of erythrodermic psoriasis and psoriatic arthritis. Although the symptoms improved, she later developed noninfectious uveitis, resulting in a sharp decline in vision. After switching to secukinumab, her vision slightly improved, her skin lesions subsided, and her joint symptoms were relieved. Given the rarity of psoriasis combined with uveitis, it is unclear whether uveitis is related to anti-TNF therapy. In addition, the selection of effective biological agents for the treatment of uveitis remains a challenge and requires extensive clinical experience.
Objective This study aimed to investigate key biomarkers and their molecular pathogenesis in psoriasis. Methods Differentially expressed genes (DEGs) of datasets (GSE13355, GSE30999, and GSE106992) obtained from Gene Expression Omnibus (GEO) were identified using Venn diagram. Function and pathway enrichment analyses were performed. Protein–protein interaction (PPI) network and the hub genes were constructed. The correlation between normal tissue and infiltrating immune cells was analyzed by CIBERSORT. ROC analysis was performed to distinguish between skin lesion samples and skin non-lesion samples. Analyze the highest expression of single gene in the whole body within the Human Protein Atlas (HPA) database. Effect of CXCL8 expression level on proliferation, invasion, migration and apoptosis of HaCat cells was detected by qPCR. Results A total of 239 pairs of normal and lesional skin samples were downloaded. PPI network revealed a tight interaction among 197 DEGs. The GO enrichment analysis showed that these genes were markedly enriched in the “defense response to virus”, “type I interferon signaling pathway”, and “cell response to type I interferon” categories. The KEGG pathway analysis showed that the DEGs were mainly in the NOD-like receptor axis, interaction between cytokine and cytokine receptor and the IL−17 axis. PPI analysis showed that CXCL8 was the novel hub gene of psoriasis and correlated to 22 types of infiltrating immune cells. 6 miRNAs were predicted to be related to CXCL8. CXCL8 was most widely distributed in lymphoid tissues and plays a role in psoriatic inflammatory lesions by promoting cell proliferation, migration, and anti-apoptosis. Conclusion CXCL8 plays a key role in psoriasis development. This study provided new insights into the exploration of molecular mechanisms and therapeutic targets of psoriasis.
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