COVID-19 Hyperinflammation: What About Neutrophils?

mSphere. 2020 Jun 24;5(3):e00367-20. doi: 10.1128/mSphere.00367-20.

Abstract

COVID-19 is often related to hyperinflammation that drives lung or multiorgan injury. The immunopathological mechanisms that cause excessive inflammation are under investigation and constantly updated. Here, a gene network approach was used on recently published data sets to identify possible COVID-19 inflammatory mechanisms and bioactive genes. First, network analysis of putative SARS-CoV-2 cellular receptors led to the mining of a neutrophil-response signature and relevant inflammatory genes. Second, analysis of RNA-seq data sets of lung cells infected with SARS-CoV-2 revealed that infected cells expressed neutrophil-attracting chemokines. Third, analysis of RNA-seq data sets of bronchoalveolar lavage fluid cells from COVID-19 patients identified upregulation of neutrophil genes and chemokines. Different inflammatory genes mined here, including TNFR, IL-8, CXCR1, CXCR2, ADAM10, GPR84, MME, ANPEP, and LAP3, might be druggable targets in efforts to limit SARS-CoV-2 inflammation in severe clinical cases. The possible role of neutrophils in COVID-19 inflammation needs to be studied further.

Keywords: COVID-19; SARS-CoV-2; coronavirus; inflammation; neutrophil.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Betacoronavirus / immunology*
  • Bronchoalveolar Lavage Fluid / cytology
  • Chemokines / genetics
  • Chemokines / immunology*
  • Coronavirus Infections / immunology*
  • Coronavirus Infections / pathology
  • Humans
  • Inflammation / immunology
  • Inflammation / pathology*
  • Lung Diseases / immunology
  • Lung Diseases / pathology
  • Neutrophil Infiltration / immunology
  • Neutrophils / immunology*
  • Pandemics
  • Pneumonia, Viral / immunology*
  • Pneumonia, Viral / pathology
  • Receptors, Virus / genetics

Substances

  • Chemokines
  • Receptors, Virus

Supplementary concepts

  • COVID-19
  • severe acute respiratory syndrome coronavirus 2