Reduced expression of SARS‐CoV‐2 host entry genes, TMPRSS2 and ACE2, in the nasal polyps of CRSwNP patients. (A) Gene expression of ACE2 and TMPRSS2 as well as proinflammatory cytokines in the inflamed uncinate tissues of CRSsNP patients (n = 3), nasal polyps of CRSwNP patients (n = 3), and uncinate tissues of healthy controls (n = 3). The data presented shows lower expression of ACE2 and TMPRSS2 in the nasal polyps of CRSwNP patients compared to normal uncinate tissue. Accordingly, gene expression levels of type 2 cytokines, IL4, IL‐5, and IL13 were higher in the nasal polyps of CRSwNP patients; whereas IL17 and IFNγ cytokines were more elevated in the uncinate tissue of CRSsNP patients. (B) Gene expression of ACE2 and TMPRSS2 as well as proinflammatory cytokines in nasal polyps of eosinophilic (n = 3), nasal polyps of non‐eosinophilic CRSwNP patients (n = 3), and sphenoid sinus mucosa of healthy controls (n = 3). The data presented shows decreased level of ACE2 and TMPRSS2 expression in the nasal polyps of eosinophilic compared to non‐eosinophilic CRSwNP patients. Additionally, it shows increased gene expression levels of type 2 cytokines, IL4, IL5, and IL13 in the nasal polyps of eosinophilic compared to non‐eosinophilic CRSwNP patients. In other hand, the gene expression levels of IL17 and IFNγ were higher in the nasal polyps of non‐eosinophilic compared to eosinophilic CRSwNP patients. (C) Gene expression level of ACE2 in the human bronchial airway epithelial BEAS‐2B cells untreated or treated with budesonide (100nM) for 18 hours. The data shows that treatment with budesonide downregulated ACE2 expression levels in the treated compared to untreated BEAS‐2B cells. (D) Gene expression level of ACE2 in bronchial biopsies from healthy male, non‐smoker, non‐allergic volunteers treated with placebo or budesonide (1600 μg). The data shows that treatment with budesonide downregulated ACE2 expression levels in the budesonide‐treated compared to placebo‐treated subjects. (E) Gene expression level of ACE2 in the primary bronchial fibroblasts untreated or treated with dexamethasone (100nM) for 24 hours. The data shows that treatment with dexamethasone downregulated ACE2 expression levels in the treated compared to untreated fibroblasts. ACE2 = angiotensin‐converting enzyme 2; CRSsNP = chronic rhinosinusitis without nasal polyps; CRSwNP = chronic rhinosinusitis with nasal polyps; IFN = interferon; IL = interleukin; TMPRSS2 = transmembrane serine protease 2.