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<p>Allergic rhinitis (AR) is a common IgE-mediated inflammatory disease, but the molecular mechanisms linking inflammation-related genes to AR progression remain incompletely understood. This study integrated bioinformatics analysis and experimental validation to identify inflammation-related candidate genes associated with AR. Differentially expressed genes were screened from the GSE19187 dataset using the limma package, while weighted gene co-expression network analysis and inflammation-related gene sets were used to identify AR-associated inflammatory genes. External validation was performed using the GSE44037 dataset, and diagnostic value was assessed by receiver operating characteristic analysis. Two candidate inflammation-related genes, SLC7A1 and TIMP1, were identified in the discovery analysis. Among them, SLC7A1 showed more consistent validation results and stronger diagnostic performance, whereas TIMP1 showed limited validation performance and was therefore considered a preliminary candidate rather than a validated biomarker. Transcription factor prediction identified NFIC as a potential shared regulator of SLC7A1 and TIMP1. In IL-13-induced JME/CF15 nasal epithelial cells, inflammatory cytokines and SLC7A1 expression were significantly increased. Functional experiments showed that, under IL-13-stimulated conditions, SLC7A1 knockdown further enhanced inflammatory cytokine production while reducing nitric oxide and inducible nitric oxide synthase levels, suggesting that IL-13-induced SLC7A1 upregulation may represent a compensatory response that helps preserve epithelial immune homeostasis. Dual-luciferase reporter and chromatin immunoprecipitation assays confirmed that NFIC directly binds to the SLC7A1 promoter and promotes its transcription. Moreover, NFIC overexpression increased SLC7A1 expression and attenuated IL-13-induced inflammatory responses. These findings suggest that SLC7A1 may have potential diagnostic relevance and may function as an inflammation-related regulator in AR, although its diagnostic utility requires further validation in larger clinical cohorts. The NFIC–SLC7A1 axis may contribute to epithelial immune regulation through arginine-dependent nitric oxide pathways and represents a potential therapeutic target for AR management.</p>

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Identification and Validation of Key Genes Related to Inflammation in Allergic Rhinitis

  • 期刊论文

  • 发表日期：

    2026年7月27日

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  • Yuncen Zhou,
  • Yun Liu,
  • Hangjun Zhu

摘要

Allergic rhinitis (AR) is a common IgE-mediated inflammatory disease, but the molecular mechanisms linking inflammation-related genes to AR progression remain incompletely understood. This study integrated bioinformatics analysis and experimental validation to identify inflammation-related candidate genes associated with AR. Differentially expressed genes were screened from the GSE19187 dataset using the limma package, while weighted gene co-expression network analysis and inflammation-related gene sets were used to identify AR-associated inflammatory genes. External validation was performed using the GSE44037 dataset, and diagnostic value was assessed by receiver operating characteristic analysis. Two candidate inflammation-related genes, SLC7A1 and TIMP1, were identified in the discovery analysis. Among them, SLC7A1 showed more consistent validation results and stronger diagnostic performance, whereas TIMP1 showed limited validation performance and was therefore considered a preliminary candidate rather than a validated biomarker. Transcription factor prediction identified NFIC as a potential shared regulator of SLC7A1 and TIMP1. In IL-13-induced JME/CF15 nasal epithelial cells, inflammatory cytokines and SLC7A1 expression were significantly increased. Functional experiments showed that, under IL-13-stimulated conditions, SLC7A1 knockdown further enhanced inflammatory cytokine production while reducing nitric oxide and inducible nitric oxide synthase levels, suggesting that IL-13-induced SLC7A1 upregulation may represent a compensatory response that helps preserve epithelial immune homeostasis. Dual-luciferase reporter and chromatin immunoprecipitation assays confirmed that NFIC directly binds to the SLC7A1 promoter and promotes its transcription. Moreover, NFIC overexpression increased SLC7A1 expression and attenuated IL-13-induced inflammatory responses. These findings suggest that SLC7A1 may have potential diagnostic relevance and may function as an inflammation-related regulator in AR, although its diagnostic utility requires further validation in larger clinical cohorts. The NFIC–SLC7A1 axis may contribute to epithelial immune regulation through arginine-dependent nitric oxide pathways and represents a potential therapeutic target for AR management.