Abstract
[Figure: see text].
Highlights
These results provide insights into the central role of NLRP3–caspase-1 pyroptotic innate immune signaling and loss of lung endothelial adherens junctions in the mechanism of acute respiratory distress syndrome induced by SARS-CoV-2
The devastating coronavirus disease 2019 (COVID19) pandemic is mediated by the SARS-CoV-2 virus, which enters host cells via direct binding of the SARS-CoV-2 spike (S)-protein to the ACE-2 receptor and TMPRSS2 membrane protease that are primarily expressed in type II lung alveolar epithelial cells.[1]
Much of the focus on SARS-CoV-2–induced lung endothelial dysfunction has been on the coagulopathy,[5,6,7] and less is known about the pathogenic role of the lung endothelium in promoting immune activation and lung edemagenesis
Summary
The data that support the findings of this study will be available from the corresponding author upon request. Mice of different ages and both sexes were intranasally inoculated with either lethal dose [plaqueforming unit]), sublethal dose (2×104 p.f.u.) of SARS-CoV-2, or. Virus inoculations were performed under anesthesia that was induced and maintained with ketamine hydrochloride and xylazine, and all efforts were made to minimize animal suffering. Biosafety level 3 experiments employing live SARS-CoV-2 were performed by personnel equipped with powered air-purifying respirators in strict compliance with the National Institutes of Health guidelines and approved by the University of Illinois Animal Care and Use Committee and the University of Illinois Institutional Biosafety Committee. Genotyping of mice was performed by polymerase chain reaction (PCR) using tail DNA. Animals with sex- and age-matched littermates were randomly included in experiments. Animal experiments were performed in a blinded fashion
Sign-in/Register to view highlights & summary 
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call