Coronavirus disease 2019, a disease caused by SARS-CoV-2, has quickly become a significant public health hazard globally. Nasal epithelial cells are an essential site for SARS-CoV-2 infection and replication. The purpose of this review is to summarize recent findings on the endotypes of CRSwNP and the potential impact of SARS-CoV-2 infection.

Endotypes of CRSwNP are characterized by type 1, type 2, and type 3 inflammation according to patterns of inflammatory cells and the cytokines expressed in nasal tissue. Nasal epithelial cells show the highest expression of angiotensin-converting enzyme 2, the receptor for attachment and entry of SARS-CoV-2 into host cells, among all investigated cells respiratory tree. SARS-CoV-2 infection likely leads to increased activation of T-helper-1 cell responses. Recent studies suggest that ACE2 may be upregulated by type 1 and downregulated by type 2 inflammatory cytokines in nasal epithelial cells.

Inflammatory endotypes of CRSwNP influence the expression of ACE2 in nasal epithelial cells. Type 1 inflammation in nasal tissue may increase the risk of SARS-CoV-2 infection by upregulating ACE2 expression. However, the clinical association between CRSwNP and COVID-19 is still unclear.