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pmid:38045687

Key genes and immune infiltration in chronic spontaneous urticaria: a study of bioinformatics and systems biology.

Wenxing Su · Yu Tian · Yuqian Wei · Fei Hao · Jiang Ji

Frontiers in immunology · 2023 doi:10.3389/fimmu.2023.1279139

Paper

complete

Experiment

complete

Data

partial

Analysis

complete

Execution

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Key genes and immune infiltration in chronic spontaneous urticaria: a study of bioinformatics and systems biology.
doi
10.3389/fimmu.2023.1279139
pmid
38045687
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[0]
Wenxing Su
[1]
Yu Tian
[2]
Yuqian Wei
[3]
Fei Hao
[4]
Jiang Ji
journal
Frontiers in immunology
year
2023
abstract
Background: Chronic spontaneous urticaria (CSU) is defined by the spontaneous occurrence of wheals and/or angioedema for >6 weeks. The pathogenesis involves skin mast cells, but the complex causes of their activation remain to be characterized in detail. Objectives: To explore disease-driving genes and biological pathways in CSU. Methods: Two microarray data sets, e.g., GSE57178 and GSE72540, with mRNA information of skin from CSU patients, were downloaded from the Gene Expression Omnibus (GEO) database. An integrated bioinformatics pipeline including identification of differentially expressed genes (DEGs), functional enrichment analysis, protein-protein interaction (PPI) network analysis, co-expression and drug prediction analysis, and immune and stromal cells deconvolution analyses were applied to identify hub genes and key drivers of CSU pathogenesis. Results: In total, we identified 92 up-regulated and 7 down-regulated genes in CSU lesions. These were significantly enriched in CSU-related pathways such as TNF, NF-κB, and JAK-STAT signaling. Based on PPI network modeling, four genes, i.e., IL-6, TLR-4, ICAM-1, and PTGS-2, were computationally identified as key pathogenic players in CSU. Immune infiltration analyses indicated that dendritic cells, Th2 cells, mast cells, megakaryocyte-erythroid progenitor, preadipocytes, and M1 macrophages were increased in lesional CSU skin. Conclusion: Our results offer new insights on the pathogenesis of CSU and suggest that TNF, NF-κB, JAK-STAT, IL-6, TLR-4, ICAM-1, and PTGS-2 may be candidate targets for novel CSU treatments.
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Spearman correlation analysis was used to explore the relationship between hub genes and infiltrating immune cells.
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Four genes, IL-6, TLR-4, ICAM-1, and PTGS-2, were computationally identified as key pathogenic players in CSU.
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Gene Expression Profiles in Chronic Idiopathic Urticaria
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Gene expression profile of patients with moderate and severe chronic spontaneous urticaria [tissue]
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and biological pathways in CSU. Methods: Two microarray data sets, e.g., GSE57178 and GSE72540, with
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Complete file
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The pathogenesis involves skin mast cells, but the complex causes of their activation remain to be characterized in detail.\nObjectives: To explore disease-driving genes and biological pathways in CSU.\nMethods: Two microarray data sets, e.g., GSE57178 and GSE72540, with mRNA information of skin from CSU patients, were downloaded from the Gene Expression Omnibus (GEO) database. An integrated bioinformatics pipeline including identification of differentially expressed genes (DEGs), functional enrichment analysis, protein-protein interaction (PPI) network analysis, co-expression and drug prediction analysis, and immune and stromal cells deconvolution analyses were applied to identify hub genes and key drivers of CSU pathogenesis.\nResults: In total, we identified 92 up-regulated and 7 down-regulated genes in CSU lesions. These were significantly enriched in CSU-related pathways such as TNF, NF-κB, and JAK-STAT signaling. Based on PPI network modeling, four genes, i.e., IL-6, TLR-4, ICAM-1, and PTGS-2, were computationally identified as key pathogenic players in CSU. Immune infiltration analyses indicated that dendritic cells, Th2 cells, mast cells, megakaryocyte-erythroid progenitor, preadipocytes, and M1 macrophages were increased in lesional CSU skin.\nConclusion: Our results offer new insights on the pathogenesis of CSU and suggest that TNF, NF-κB, JAK-STAT, IL-6, TLR-4, ICAM-1, and PTGS-2 may be candidate targets for novel CSU treatments.", "claims": [{"id": "claim-method", "statement": "Spearman correlation analysis was used to explore the relationship between hub genes and infiltrating immune cells.", "kind": "methodological", "target": null, "evidence": [{"asset": "source:pmid:38045687", "locator": "sections[9] \"Correlation analysis of hub genes and infiltrating immune cells\" paragraph 2", "quote": "Spearman correlation analysis was used to explore the relationship between hub genes and infiltrating immune cells."}], "state": "complete"}, {"id": "claim-data-access", "statement": "The datasets presented in this study can be found in online repositories. 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