Comprehensive analysis reveals hub genes associated with immune cell infiltration in allergic rhinitis

• Published in: World journal of otorhinolaryngology - head and neck surgery Vol. 9; no. 4; pp. 340 - 351
• Main Authors: Li, Hui, Huang, Shi‐En, Geng, Cong‐Li, Wu, Yu‐Xiao, Shi, Mu‐Han, Wang, Min
• Format: Journal Article
• Language: English
• Published: United States John Wiley & Sons, Inc 01.12.2023; John Wiley and Sons Inc; Wiley
• Subjects: allergic rhinitis; Cells; CIBERSORT; consensus cluster; Cytokines; Datasets; Disease; Gene expression; GSEA; GSVA; Hay fever; immune cell infiltration; Neutrophils; Pathogenesis; Proteins; Research Paper; Research Papers; Rhinitis; Software; WGCNA; immune cell infiltration; CIBERSORT; GSVA; GSEA; consensus cluster; allergic rhinitis; WGCNA
• ISSN: 2095-8811; 2589-1081
• DOI: 10.1002/wjo2.92

Objectives Allergic rhinitis (AR) refers to a form of respiratory inflammation that mainly affects the sinonasal mucosa. The purpose of this study was to explore the level of immune cell infiltration and the pathogenesis of AR. Methods We performed a comprehensive analysis of two gene expression profiles (GSE50223 and GSE50101, a total of 30 patients with AR and 31 healthy controls). CIBERSORT was used to evaluate the immune cell infiltration levels. Weighted gene coexpression network analysis was applied to explore potential genes or gene modules related to immune status, and enrichment analyses including gene ontology, Kyoto Encyclopedia of Genes and Genomes, gene set enrichment analysis, and gene set variation analysis, were performed to analyze the potential mechanisms in AR. A protein–protein interaction network was constructed to investigate the hub genes, and consensus clustering was conducted to identify the molecular subtypes of AR. Results Compared to the healthy controls, patients with AR had high abundance levels and proportions of CD4+ memory‐activated T cells. One hundred and eight immune‐related differentially expressed genes were identified. Enrichment analysis suggested that AR was mainly related to leukocyte cell‐cell adhesion, cytokine‐cytokine receptor interaction, T‐cell activation, and T‐cell receptor signaling pathway. Ten hub genes, including TYROBP, CSF1R, TLR8, FCER1G, SPI1, ITGAM, CYBB, FCGR2A, CCR1, and HCK, which were related to immune response, might be crucial to the pathogenesis of AR. Three molecular subtypes with significantly different immune statuses were identified. Conclusion This study improves our understanding of the molecular mechanisms in AR via comprehensive strategies and provides potential diagnostic biomarkers and therapeutic targets of AR. Flow chart of this study. Highlights Reveal the details of immune cell infiltration in allergic rhinitis (AR) and in its subtypes. Identify the related biological pathways and hub genes involved in the development of AR. Provide potential diagnostic biomarkers and therapeutic targets of AR.