The nasal symbiont Staphylococcus species restricts the transcription of SARS-CoV-2 entry factors in human nasal epithelium
Jeong-Yeon Ji,
Ara Jo,
Jina Won,
Chan Hee Gil,
Haeun Shin,
Sujin Kim,
Yung Jin Jeon,
Hyun Jik Kim
Affiliations
Jeong-Yeon Ji
Seoul National University Hospital, Seoul, Korea
Ara Jo
Department of Otorhinolaryngology, Seoul National University College of Medicine, 103 Daehak-ro, Jongno-gu, 110-799 Seoul, Korea
Jina Won
Department of Otorhinolaryngology, Seoul National University College of Medicine, 103 Daehak-ro, Jongno-gu, 110-799 Seoul, Korea
Chan Hee Gil
Department of Otorhinolaryngology, Seoul National University College of Medicine, 103 Daehak-ro, Jongno-gu, 110-799 Seoul, Korea
Haeun Shin
Department of Otorhinolaryngology, Seoul National University College of Medicine, 103 Daehak-ro, Jongno-gu, 110-799 Seoul, Korea
Sujin Kim
Department of Otorhinolaryngology, Seoul National University College of Medicine, 103 Daehak-ro, Jongno-gu, 110-799 Seoul, Korea
Yung Jin Jeon
Department of Otorhinolaryngology, Gyeongsang National University Hospital, Jinju, Korea
Hyun Jik Kim
Department of Otorhinolaryngology, Seoul National University College of Medicine, 103 Daehak-ro, Jongno-gu, 110-799 Seoul, Korea; Seoul National University Hospital, Seoul, Korea; Corresponding author
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.