Short Note
Version 1
Preserved in Portico This version is not peer-reviewed
A Neutrophil Activation Signature in COVID-19
Version 1
: Received: 18 April 2020 / Approved: 20 April 2020 / Online: 20 April 2020 (12:38:59 CEST)
Version 2 : Received: 22 April 2020 / Approved: 22 April 2020 / Online: 22 April 2020 (06:23:01 CEST)
Version 2 : Received: 22 April 2020 / Approved: 22 April 2020 / Online: 22 April 2020 (06:23:01 CEST)
How to cite: Didangelos, A. A Neutrophil Activation Signature in COVID-19. Preprints 2020, 2020040363. https://doi.org/10.20944/preprints202004.0363.v1 Didangelos, A. A Neutrophil Activation Signature in COVID-19. Preprints 2020, 2020040363. https://doi.org/10.20944/preprints202004.0363.v1
Abstract
Covid-19 is often related to hyperinflammation that drives lung or multi-organ damage and mortality. The immunopathological mechanisms that cause excessive inflammation following SARS-Cov-2 infection are under investigation while different approaches to limit hyperinflammation in affected patients are being proposed. Here, a computational network approach was used on recently available data to identify possible Covid-19 inflammatory mechanisms. First, network analysis of putative SARS-Cov-2 cellular receptors and their directly associated interacting proteins, led to the mining of a robust neutrophil-response signature and multiple relevant inflammatory response genes. Second, analysis of RNA-seq datasets of lung epithelial cells infected with SARS-Cov-2 found that infected cells specifically expressed neutrophil-attracting chemokines, further supporting the likely role of neutrophils in Covid-19 inflammation. The role of neutrophils in Covid-19 needs to be studied further. Different immunoregulatory molecules and pathways presented here (TNF Receptor, IL8, CXCR1, CXCR2, ADAM10, GPR84, MME-neprilysin, ANPEP, LAP3) are druggable and might be therapeutic targets in efforts to limit SARS-Cov-2 inflammation in severe clinical cases.
Keywords
Covid-19; SARS-Cov-2; inflammation; neutrophil
Subject
Biology and Life Sciences, Immunology and Microbiology
Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Comments (0)
We encourage comments and feedback from a broad range of readers. See criteria for comments and our Diversity statement.
Leave a public commentSend a private comment to the author(s)
* All users must log in before leaving a comment
