AI Article Synopsis
- SARS-CoV-2 infection has been identified as a pandemic, with severe cases showing significant inflammation and lung damage.
- A study re-analyzed scRNA-seq data from COVID-19 patients, revealing that those with severe symptoms exhibited epithelial cell DNA damage and increased neutrophil infiltration.
- The findings indicate that proinflammatory factors and glucocorticoid receptor expression play a key role in the severity of COVID-19 symptoms, linking neutrophil activity to the inflammatory response in the lungs.
Article Abstract
SARS-CoV-2 infection has recently been declared a pandemic. Some patients showing severe symptoms exhibit drastic inflammation and airway damage. In this study, we re-analyzed published scRNA-seq data of COVID-19 patient bronchoalveolar lavage fluid to further classify and compare immunological features according to the patient's disease severity. Patients with severe symptoms showed DNA damage and apoptotic features of epithelial cells. Our results suggested that epithelial damage was associated with neutrophil infiltration. Myeloid cells of severe patients showed higher expression of proinflammatory cytokines and chemokines such as CXCL8. As a result, neutrophils were abundant in lungs of patients from the severe group. Furthermore, recruited neutrophils highly expressed genes related to neutrophil extracellular traps. Neutrophil-mediated inflammation was regulated by glucocorticoid receptor expression and activity. Based on these results, we suggest that severe COVID-19 symptoms may be determined by differential expression of glucocorticoid receptors and neutrophils.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7485000 | PMC |
| http://dx.doi.org/10.3389/fimmu.2020.02145 | DOI Listing |
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