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

Research output: Contribution to journal › Journal article › Research › peer-review

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Experimental Model of Pulmonary Inflammation Induced by SARS-CoV-2 Spike Protein and Endotoxin. / Puthia, Manoj; Tanner, Lloyd; Petruk, Ganna; Schmidtchen, Artur.

In: ACS Pharmacology and Translational Science, Vol. 5, No. 3, 11.03.2022, p. 141-148.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Puthia, M, Tanner, L, Petruk, G & Schmidtchen, A 2022, 'Experimental Model of Pulmonary Inflammation Induced by SARS-CoV-2 Spike Protein and Endotoxin', ACS Pharmacology and Translational Science, vol. 5, no. 3, pp. 141-148. https://doi.org/10.1021/acsptsci.1c00219

APA

Puthia, M., Tanner, L., Petruk, G., & Schmidtchen, A. (2022). Experimental Model of Pulmonary Inflammation Induced by SARS-CoV-2 Spike Protein and Endotoxin. ACS Pharmacology and Translational Science, 5(3), 141-148. https://doi.org/10.1021/acsptsci.1c00219

Vancouver

Puthia M, Tanner L, Petruk G, Schmidtchen A. Experimental Model of Pulmonary Inflammation Induced by SARS-CoV-2 Spike Protein and Endotoxin. ACS Pharmacology and Translational Science. 2022 Mar 11;5(3):141-148. https://doi.org/10.1021/acsptsci.1c00219

Author

Puthia, Manoj ; Tanner, Lloyd ; Petruk, Ganna ; Schmidtchen, Artur. / Experimental Model of Pulmonary Inflammation Induced by SARS-CoV-2 Spike Protein and Endotoxin. In: ACS Pharmacology and Translational Science. 2022 ; Vol. 5, No. 3. pp. 141-148.

Bibtex

@article{fe27aeb3983244a487c86c6fcc71df03,

title = "Experimental Model of Pulmonary Inflammation Induced by SARS-CoV-2 Spike Protein and Endotoxin",

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.",

keywords = "ARDS, COVID-19 in vivo models, LPS, SARS-CoV-2 spike (S) protein, TCP-25",

author = "Manoj Puthia and Lloyd Tanner and Ganna Petruk and Artur Schmidtchen",

note = "Publisher Copyright: {\textcopyright} 2022 The Authors. Published by American Chemical Society",

year = "2022",

month = mar,

day = "11",

doi = "10.1021/acsptsci.1c00219",

language = "English",

volume = "5",

pages = "141--148",

journal = "ACS Pharmacology and Translational Science",

issn = "2575-9108",

publisher = "ACS Publications",

number = "3",

}

RIS

TY - JOUR

T1 - Experimental Model of Pulmonary Inflammation Induced by SARS-CoV-2 Spike Protein and Endotoxin

AU - Puthia, Manoj

AU - Tanner, Lloyd

AU - Petruk, Ganna

AU - Schmidtchen, Artur

PY - 2022/3/11

Y1 - 2022/3/11

N2 - 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.

AB - 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.

KW - ARDS

KW - COVID-19 in vivo models

KW - LPS

KW - SARS-CoV-2 spike (S) protein

KW - TCP-25

UR - http://www.scopus.com/inward/record.url?scp=85124131709&partnerID=8YFLogxK

U2 - 10.1021/acsptsci.1c00219

DO - 10.1021/acsptsci.1c00219

M3 - Journal article

C2 - 35774232

AN - SCOPUS:85124131709

VL - 5

SP - 141

EP - 148

JO - ACS Pharmacology and Translational Science

JF - ACS Pharmacology and Translational Science

SN - 2575-9108

IS - 3

ER -

ID: 316682361

Department of Biomedical Sciences