Experimental Model of Pulmonary Inflammation Induced by SARS-CoV-2 Spike Protein and Endotoxin

Research output: Contribution to journalArticlepeer-review

Abstract

COVID-19 is characterized by a dysregulated and excessive inflammatory response and, in severe cases, acute respiratory distress syndrome. We have recently demonstrated a previously unknown high-affinity interaction between the SARS-CoV-2 spike (S) protein and bacterial lipopolysaccharide (LPS), leading to the boosting of inflammation. Here we present a mouse inflammation model employing the coadministration of aerosolized S protein together with LPS to the lungs. Using NF-κB-RE-Luc reporter and C57BL/6 mice followed by combinations of bioimaging, cytokine, chemokine, fluorescence-activated cell sorting, and histochemistry analyses, we show that the model yields severe pulmonary inflammation and a cytokine profile similar to that observed in COVID-19. Therefore, the model offers utility for analyses of the pathophysiological features of COVID-19 and the development of new treatments.

Original languageEnglish
Pages (from-to)141-148
Number of pages8
JournalACS Pharmacology and Translational Science
Volume5
Issue number3
DOIs
Publication statusPublished - 2022 Mar

Subject classification (UKÄ)

  • Immunology in the medical area

Keywords

  • ARDS
  • COVID-19 in vivo models
  • LPS
  • SARS-CoV-2 spike (S) protein
  • TCP-25

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