Preprint Short Note Version 1 Preserved in Portico This version is not peer-reviewed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)

How to cite: Didangelos, A. A Neutrophil Activation Signature in COVID-19. Preprints 2020, 2020040363 (doi: 10.20944/preprints202004.0363.v1). Didangelos, A. A Neutrophil Activation Signature in COVID-19. Preprints 2020, 2020040363 (doi: 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.

Subject Areas

Covid-19; SARS-Cov-2; inflammation; neutrophil

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