We can perform pre-clinincal studies around SARS-CoV-2, thereby contibuting to research and therapy development to halt this virus. We do this using, amongst others, SARS-CoV-2 spike protein, UV-inactivated SARS-CoV-2 virus or inflammatory stimuli to model the airway inflammation/cytokine storm that is observed. We cannot work with the active virus.

We have worked with the following models:

Epithelial cells, which are shown to express ACE-2 and to be susceptive for SARS-CoV-2 infection. This includes primary epithelial cells and Calu-3 cells.
Endothelial cells, including HPMEC cells, can be of interest to study vascular permeability.

We set up a lung slice model using a cytokine cocktail relevant for SARS-Cov-2-induced cytokine storm, including IL-6, IL-1B and TNF-a, which results in a strong and reproducible inflammatory response evaluated at 48h.

Mouse organoid cultures can be treated with the different stimuli relevant for SARS-CoV-2 infection, and the impact of potential therapies on fibroblast-epithelial interactions and epithelial repair can be studied.

LPS is a known stimulus to induce lung inflammation and ARDS-like characteristics. We have mouse and guinea pig models available, including only one time exposure models, making these models relatively fast.