基于生物信息学分析与验证慢性自发性荨麻疹的免疫相关枢纽基因OA

Objective This study aims to systematically screen immune-related hub genes in chronic spontaneous urticaria(CSU)and explore their underlying immune molecular mechanisms by integrating bioinformatics analysis with experimental validation.Methods Microarray datasets(GSE72540)of CSU were downloaded from the Gene Expression Omnibus(GEO)database.Differentially expressed genes(DEGs)were screened using the GEO2R online analysis tool and intersected with an immune-related gene set to obtain differentially expressed immune genes(DEIGs).Subsequently,Gene Ontology(GO)enrichment analysis,Kyoto Encyclopedia of Genes and Genomes(KEGG)pathway enrichment analysis,and protein-protein interaction(PPI)network construction were performed for the DEIGs.The CytoHubba plugin of Cytoscape software was used to screen hub genes.Plasma samples were collected from 11 patients with CSU and 9 healthy controls,and the mRNA expression levels of key genes were detected and compared by quantitative real-time PCR.Results A total of 93 DEIGs were identified.Enrichment analysis revealed these genes were significantly enriched in immune-related processes such as leukocyte migration,chemotaxis,cytokine-cytokine receptor interaction,IL-17 signaling pathway,and nuclear factor-kappa B(NF-κB)signaling pathway.Six hub genes[C-C motif chemokine ligand 2(CCL2),IL-1β,Cluster of Differentiation 86(CD86),Tumor Necrosis Factor(TNF),C-X-C motif chemokine ligand 1(CXCL1),and Prostaglandin-endoperoxide Synthase 2(PTGS2)]were screened from the PPI network.Clinical validation showed that,compared with healthy controls,the plasma mRNA expression levels of IL-1 β and PTGS2 were upregulated in CSU patients(both P＜0.05),while no statistically significant differences were observed in the mRNA expression levels of CCL2,CD86,TNF,or CXCL1(all P＞0.05).Conclusion IL-1β and PTGS2 are key immune-related hub genes in CSU,likely playing crucial roles in the pathogenesis of CSU by regulating complex inflammatory networks.They show promise as potential diagnostic biomarkers or novel therapeutic targets for CSU.