{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,9]],"date-time":"2026-04-09T18:08:35Z","timestamp":1775758115621,"version":"3.50.1"},"reference-count":68,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2024,9,10]],"date-time":"2024-09-10T00:00:00Z","timestamp":1725926400000},"content-version":"vor","delay-in-days":9,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal of Medical Virology"],"published-print":{"date-parts":[[2024,9]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>This study aimed to investigate the impact of different types of nasal inflammation on the regulation of entry\u2010associated genes of respiratory viruses, including severe acute respiratory syndrome coronavirus 2 (SARS CoV\u20102), Middle East respiratory syndrome coronavirus (MERS\u2010CoV), human coronavirus 229E (HCoV\u2010229E), and influenza virus, in the nasal epithelium. Subjects were classified into three groups: control, eosinophilic chronic rhinosinusitis (ECRS), and noneosinophilic CRS (NECRS) groups. Angiotensin\u2010converting enzyme 2 (ACE2) and transmembrane protease serine subtype 2 (TMPRSS2), alanyl aminopeptidase (ANPEP), dipeptidyl peptidase 4 (DPP4), and beta\u2010galactoside alpha\u20102,6\u2010sialyltransferase 1 (ST6GAL1), and beta\u2010galactoside alpha\u20102,3\u2010sialyltransferase 4 (ST3GAL4) were selected as key entry\u2010associated genes for SARS\u2010CoV\u20102, HCoV\u2010229E, MERS\u2010CoV, and influenza, respectively, and were evaluated. Brushing samples obtained from each group and human nasal epithelial cells cultured using an air\u2013liquid interface system were treated for 7 days with typical inflammatory cytokines and analyzed using real\u2010time polymerase chain reaction. Western blot analysis and confocal microscopy were performed. The entry\u2010associated genes showed distinct regulation patterns in response to each interleukin\u20104 (IL\u20104), interleukin\u201013 (IL\u201013), tumor necrosis factor\u2010\u03b1 (TNF\u2010\u03b1), and interferon\u2010\u03b3 (IFN\u2010\u03b3). Specifically, ACE2 significantly decreased in type 2 cytokines (IL\u20104 and IL\u201013), while TMPRSS2 significantly decreased in type 1 cytokines (TNF\u2010\u03b1 and IFN\u2010\u03b3). ANPEP significantly decreased in both types of cytokines. Remarkably, DPP4 significantly increased in type 2 cytokines and decreased in type 1 cytokines. Moreover, ST6GAL1 and ST3GAL4 significantly increased in type 2 cytokines and decreased in type 1 cytokines, particularly IFN\u2010\u03b3. These findings were supported by western blot analysis and confocal imaging results, especially for ACE2 and DPP4. The findings regarding differential regulation suggest that patients with ECRS, primarily mediated by type 2 inflammation, may have lower susceptibility to SARS\u2010CoV\u20102 and HCoV\u2010229E infections but higher susceptibility to MERS\u2010CoV and influenza infections.<\/jats:p>","DOI":"10.1002\/jmv.29913","type":"journal-article","created":{"date-parts":[[2024,9,11]],"date-time":"2024-09-11T01:48:44Z","timestamp":1726019324000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["Differential regulation of viral entry\u2010associated genes modulated by inflammatory cytokines in the nasal epithelium"],"prefix":"10.1002","volume":"96","author":[{"given":"Hae Eun","family":"Noh","sequence":"first","affiliation":[{"name":"Department of Otorhinolaryngology Yonsei University College of Medicine  Seoul Republic of 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