Identification of Susceptibility Genes to Allergic Rhinitis by Gene Expression Data Sets

Abstract

As an extremely prevalent disease worldwide, allergic rhinitis (AR) is a condition characterized by chronic inflammation of the nasal mucosa. To identify the finer molecular mechanisms associated with the AR susceptibility genes, differentially expressed genes (DEGs) in AR were investigated. The DEG expression and clinical data of the GSE19187 data set were used for weighted gene co‐expression network analysis (WGCNA). After the modules related to AR had been screened, the genes in the module were extracted for Gene Ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis, whereby the genes enriched in the KEGG pathway were regarded as the pathway‐genes. The DEGs in patients with AR were subsequently screened out from GSE19187, and the sensitive genes were identified in GSE18574 in connection with the allergen challenge. Two kinds of genes were compared with the pathway‐genes in order to screen the AR susceptibility genes. Receiver operating characteristic (ROC) curve was plotted to evaluate the capability of the susceptibility genes to distinguish the AR state. Based on the WGCNA in the GSE19187 data set, 10 co‐expression network modules were identified. The correlation analyses revealed that the yellow module was positively correlated with the disease state of AR. A total of 89 genes were found to be involved in the enrichment of the yellow module pathway. Four genes (CST1, SH2D1B, DPP4, and SLC5A5) were upregulated in AR and sensitive to allergen challenge, whose potentials were further confirmed by ROC curve. Taken together, CST1, SH2D1B, DPP4, and SLC5A5 are susceptibility genes to AR.

Differential modulation of allergic rhinitis nasal transcriptome by dupilumab and allergy immunotherapy

“…CCL26, encoding eotaxin-3, is also driven by IL-4 and IL-13 and has well-established roles in AD, EoE, asthma, and CRSwNP. [48][49][50][51][52] Together, these data suggest that patients with seasonal AR may have underlying chronic type 2 inflammation and emphasize that similar molecular pathophysiologic mechanisms exist across type 2 inflammatory diseases involving different tissues and organ systems. 32 NAC has been extensively used in clinical trials and in mechanistic research studying AR disease.…”

DPP4 Inhibitor Sitagliptin Reduces Inflammatory Responses and Mast Cell Activation in Allergic Rhinitis

“…Furthermore, in a retrospective study, excluding a history of AR and DPP4 inhibitor treatment, Asian patients with diabetes treated with a DPP4 inhibitor within 3 years had a significantly lower risk of developing AR (diagnosed according to ICD-9 codes) [6]. Besides, DPP4 has been recognized as a susceptibility gene for AR [7]. These data indicate that DPP4 is closely associated with AR.…”

“…The expression level of DPP4 in peripheral blood of AR is increased. Novelty, DPP4 stands out among numerous genes in the GSE19187 dataset based on weighted gene co-expression network analysis and ROC curve validation, and is regarded as one of the most sensitive genes for AR with great potential [7]. The pathogenesis of AR is mainly related to the imbalance of the immune system, and T lymphocytes are crucial in the sensitization and pathogenic stages.…”

Immunogenetic Predictors of Allergic Rhinitis

“…В одному із останніх досліджень [16] були з'ясовані молекулярні механізми, що лежать в основі прогресування АР. Підвищений ризик АР пов'язаний з генами, які регулюють імунну відповідь, такими як TLR4 і CD14.…”