Experimental Model of Pulmonary Inflammation Induced by SARS-CoV-2 Spike Protein and Endotoxin
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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 language | English |
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Journal | ACS Pharmacology and Translational Science |
Volume | 5 |
Issue number | 3 |
Pages (from-to) | 141-148 |
Number of pages | 8 |
ISSN | 2575-9108 |
DOIs | |
Publication status | Published - 11 Mar 2022 |
Bibliographical note
Publisher Copyright:
© 2022 The Authors. Published by American Chemical Society
- ARDS, COVID-19 in vivo models, LPS, SARS-CoV-2 spike (S) protein, TCP-25
Research areas
ID: 316682361