摘要：SummaryEmerging evidence indicates that severe acute respiratory syndrome-related coronavirus-2 (SARS-CoV-2) is transmitted through the human nasal mucosa via the principal entry factors angiotensin-converting enzyme 2 (ACE2) and transmembrane serine protease 2 (TMPRSS2), which are highly expressed in the nasal epithelium. Therefore, the biologics targeting host entry factors on human nasal mucosa will be necessary for complete control of SARS-CoV-2. Our data reveal thatACE2was more abundant in human nasal mucosa than lung tissue. BothACE2andTMPRSS2transcriptions significantly decreased in nasal epithelium in response toS. epidermidisand were relatively lower in human nasal mucus with large numbers ofS. epidermidis.ACE2transcription was also reduced in nasal epithelium in response to nasal symbiontS. aureus. This study proposes thatStaphylococcus speciesnasal commensals might potentially restrict SARS-CoV-2 entry to the nasal epithelium via down regulation of cellular receptors coupled with reduction of principal host protease.Graphical abstractDisplay OmittedHighlights•The cellular receptor of SARS-CoV-2 was more distributed in human nasal mucosa•Human nasal epithelium is the primary target of SARS-CoV-2 transmission•Staphylococcus speciesreduce the transcription of SARS-CoV-2 entry factors•Nasal symbionts impede the cellular invasion of SARS-CoV-2 into human nasal epitheliumBiological sciences; Molecular biology; Microbiology; Virology
