Key genes and immune infiltration in chronic spontaneous urticaria: a study of bioinformatics and systems biology
作者全名:"Su, Wenxing; Tian, Yu; Wei, Yuqian; Hao, Fei; Ji, Jiang"
作者地址:"[Su, Wenxing; Ji, Jiang] Soochow Univ, Affiliated Hosp 2, Dept Dermatol, Suzhou, Peoples R China; [Su, Wenxing; Hao, Fei] Chongqing Med Univ, Affiliated Hosp 3, Dermatol & Plast Surg Ctr, Chongqing, Peoples R China; [Tian, Yu] Chengdu Med Coll, Affiliated Hosp 1, Dept Dermatol, Chengdu, Peoples R China; [Wei, Yuqian] Nantong Third Peoples Hosp, Dept Nephropathy, Nantong, Peoples R China"
通信作者:"Ji, J (通讯作者),Soochow Univ, Affiliated Hosp 2, Dept Dermatol, Suzhou, Peoples R China.; Hao, F (通讯作者),Chongqing Med Univ, Affiliated Hosp 3, Dermatol & Plast Surg Ctr, Chongqing, Peoples R China."
来源:FRONTIERS IN IMMUNOLOGY
ESI学科分类:IMMUNOLOGY
WOS号:WOS:001110376000001
JCR分区:Q1
影响因子:5.7
年份:2023
卷号:14
期号:
开始页:
结束页:
文献类型:Article
关键词:chronic spontaneous urticaria; bioinformatics; differentially expressed genes; hub genes; pathway; immune infiltration; TNF; NF-kappa B
摘要:"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-kappa B, 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-kappa B, JAK-STAT, IL-6, TLR-4, ICAM-1, and PTGS-2 may be candidate targets for novel CSU treatments."
基金机构:National Natural Science Foundation of China10.13039/501100001809 [69]
基金资助正文:A preprint of the study has been published (https://www.researchsquare.com/article/rs-137346/v1) (69).