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.
You can read more information on the different models on the specific sub-pages. Furthermore, feel free to reach out with additional questions. We’re eager to contribute to potential solutions to halt this virus.