Distinct gene expression profiles and regulation networks of nasal polyps in eosinophilic and non‐eosinophilic chronic rhinosinusitis

<jats:sec><jats:title>Background</jats:title><jats:p>Chronic rhinosinusitis with nasal polyps (CRSwNP) is known to have 2 phenotypes in East Asia. Eosinophilic CRSwNP (ECRSwNP), defined as tissue eosinophilia and easily recurrent, is distinguished from other non‐eosinophilic CRSwNP (NECRSwNP) types. However, the pathogenesis of each remains unclear.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p>Nasal polyp tissues from ECRS (ECRSwNP) and NECRS (NECRSwNP) patients were obtained, and their comprehensive gene expression profiles were investigated by microarray analysis. Bioinformatics approaches (eg, Ingenuity Pathway Analysis [IPA]) were used to interrogate the data sets.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p>Hierarchical clustering and principal component analysis (PCA) collectively showed that ECRSwNP and NECRSwNP had distinct gene expression patterns. Of note, these genes could be divided into 8 distinctive clusters having different expression patterns and functions. Upstream Regulator Analysis revealed that not only T‐helper 2 (Th2) and the eosinophilia–related molecules (interleukin 4 [IL4], IL5, and colony stimulating factor 2 [CSF2]) reported so far, but also cell cycle regulators (cyclin dependent kinase inhibitor 1A [CDKNA1] and cyclin D1 [CCND1]) and a tissue fibrosis–related molecule (transforming growth factor β [TGFβ]) were identified in ECRSwNP. On the other hand, mainly interferons (IFNs) and acute inflammatory cytokines (IL1 and IL6) were predicted as upstream regulators in NECRSwNP.</jats:p></jats:sec><jats:sec><jats:title>Conclusion</jats:title><jats:p>These results are useful for understanding the molecular basis of the mechanisms of CRSwNP and point to new targets for developing specific biomarkers and personalized therapeutic strategies for CRSwNP.</jats:p></jats:sec>