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B. Yang - J-Q. Zhang - Y. Yuan - M. Gu - C. Hong - C-Y. Qiu - X-Y. Zou - M-P. Lu - L. Cheng

DOI: 10.4193/Rhin24.462

BACKGROUND: Emerging evidence has highlighted a potential link between chronic rhinosinusitis with nasal polyps (CRSwNP) and coronavirus disease 2019 (COVID-19). However, the exact mechanism driving this association is not well understood. We aimed
to explore the biological pathways and differentially expressed genes (DEGs) involved in CRSwNP and COVID-19 by performing bioinformatic analyses. METHODS: Data from the GEO database was analyzed using the “limma” package to identify DEGs. Techniques
like weighted gene co-expression network analysis (WGCNA), protein-protein interaction (PPI) networks, and machine learning were employed to pinpoint key genes. Single-sample gene set enrichment analysis (ssGSEA) was used to assess immune
cell infiltration. Key gene expression in macrophages was verified using single-cell analysis and immunofluorescence. Genetranscription factor-microRNA (gene-TF-miRNA) regulatory networks were constructed via NetworkAnalyst. Potential therapeutic
agents were identified through DGIdb. Nasal polyps and control nasal tissues were surgically obtained for validation purposes. RESULTS: The findings revealed 19 co-DEGs common to both CRSwNP and COVID-19, which were enriched in pathways related to
inflammation and the immune response. Among these genes, CD163 was identified as the key gene. The infiltration of CD163+ macrophages was substantially greater in the nasal tissues of CRSwNP and COVID-19 patients than in those of control subjects.
Fluticasone was determined to be a promising drug that targets CD163. CONCLUSION: This study highlights CD163 as a promising diagnostic marker for CRSwNP and COVID-19, suggesting that targeting CD163 may be pivotal in the management of these
conditions.

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