The Coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV2), becomes a global threat to humanity. In severe COVID-19 patients, excessive proinflammatory responses and impaired host immune system are observed which could result in the progression of acute respiratory distress syndrome (ARDS) and even death.

In-depth investigation of SARS-CoV-2 infected cell types, the consequent host immune response, and the communication patterns between infected cells and immune system could facilitate the identification of COVID-19 patients and their optimal treatments.

By analyzing single-cell RNA sequencing data of bronchoalveolar lavage fluid samples from COVID-19 patients and healthy donors, this study revealed high expression of SARS-CoV-2 receptor ACE2 and TMPRSS2 in lung epithelial cells of COVID-19 patients, in particular club and ciliated cells. SARS-CoV-2 infection induced pro-inflammatory genes expression and interferon/cytokine signaling in these cells.

In severe COVID-19 patients, remarkably high neutrophil but low macrophage cells in lung were observed along with excessive expressions of cytokines. Moreover, SARS-CoV-2 infection altered the community interplays among lung epithelial and immune cells, and the dysregulated cytokine/receptor interactions were correlated with severity of COVID-19.

the study identified critical cell type, dysregulated immunity and their interactions in the lung of SARS-CoV-2 infection, thus provided new insight into the mechanisms underlying of SARSCoV-2 infection in COVID-19 patients.