Re-analysis of Single Cell Transcriptome Reveals That the NR3C1-CXCL8-Neutrophil Axis Determines the Severity of COVID-19

Título

Re-analysis of Single Cell Transcriptome Reveals That the NR3C1-CXCL8-Neutrophil Axis Determines the Severity of COVID-19

Autor

Heung Kyu Lee, Jang Hyun Park, Heung Kyu Lee

Descripción

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.

Fecha

2020

Materia

covid-19, SARS-CoV-2, neutrophil, glucocorticoid, BAL, CXCL8

Identificador

10.3389/fimmu.2020.02145

Fuente

Epidemiology and Health

Editor

Korean Society of Epidemiology

Cobertura

Immunologic diseases. Allergy

Archivos

https://socictopen.socict.org/files/to_import/pdfs/696cfc8a90fa4f8b06acc7701a96c600.pdf

Colección

Citación

Heung Kyu Lee, Jang Hyun Park, Heung Kyu Lee, “Re-analysis of Single Cell Transcriptome Reveals That the NR3C1-CXCL8-Neutrophil Axis Determines the Severity of COVID-19,” SOCICT Open, consulta 18 de abril de 2026, https://www.socictopen.socict.org/items/show/5748.

Formatos de Salida

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