The nasal symbiont Staphylococcus species restricts the transcription of SARS-CoV-2 entry factors in human nasal epithelium

Highlights

• 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 species reduce the transcription of SARS-CoV-2 entry factors

• Nasal symbionts impede the cellular invasion of SARS-CoV-2 into human nasal epithelium

Summary

Emerging 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 that ACE2 was more abundant in human nasal mucosa than lung tissue. Both ACE2 and TMPRSS2 transcriptions significantly decreased in nasal epithelium in response to S. epidermidis and were relatively lower in human nasal mucus with large numbers of S. epidermidis. ACE2 transcription was also reduced in nasal epithelium in response to nasal symbiont S. aureus. This study proposes that Staphylococcus species nasal 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.