There has been incredible scientific effort and progress over the past two years geared at the protection and treatment of COVID-19. On the preclinical side, developing translational COVID-19 models that closely mimic the clinical progression of the disease is vital to understand the disease and how we can treat patients effectively. The challenges in developing such models are numerous. They include infecting and replicating SARS-CoV-2 in host subjects, developing clinical characteristics of COVID-19, and ensuring that the research model is reproducible.
In this blog, we will highlight some significant recent advances in SARS-CoV-2 preclinical modelling, which use the inExpose to deliver inhaled target compounds and the flexiVent to characterize a full pulmonary function profile.
Preclinical efficacy and safety of novel SNAT against SARS–CoV–2 using a hamster model. (2022). Pokhrel, L.R., et al. Drug Delivery and Translational Research, 849
Syrian hamsters as a model of lung injury with SARS–CoV–2 infection: Pathologic, physiologic, and detailed molecular profiling. (2022) Bednash, J.S., et al. Translational Research 240, 1-16
Ultrapotent miniproteins targeting the receptor-binding domain protect against SARS-CoV-2 infection and disease in mice. (2021). Case, J., et al. Cell Host Microbe, 29(7): 1151-1161
Role of angiotensin-converting enzyme 2 in fine particulate matter-induced acute lung injury. (2022). Zhu, P. et al. Science of the Total Environment, 825, 153964
Alveolar regeneration following viral infection is independent of tuft cells. (2022). Huang, H., et al. bioRxiv, https://doi.org/10.1101/2022.03.11.483948
Eucalyptol inhaled during Invasive Mechanical Ventilation may attenuate Lung Injury caused by oxygen therapy in the management of COVID-19. (2022) Serra, D.S., et al. Australian Journal of Basic and Applied Sciences 16(4): 1-10
SARS–CoV–2 infection of human ACE2-transgenic mice causes severe lung inflammation and impaired function. (2020). Winkler, E.S. et al (2020). Nature Immunology volume 21, pages1327–1335
Loss of furin cleavage site attenuates SARS–CoV–2 pathogenesis. (2021). Johnson, B.A et al. Nature volume 591, pages293–299
SARS–CoV–2 infection in the lungs of human ACE2 transgenic mice causes severe inflammation, immune cell infiltration, and compromised respiratory function. (2020). Winkler, E.S., et al. BioRxiv, doi: https://doi.org/10.1101/2020.07.09.196188
E-cigarette-induced pulmonary inflammation and dysregulated repair are mediated by nAChR α7 receptor: role of nAChR α7 in SARS-CoV-2 Covid-19 ACE2 receptor regulation. (2020). Wang, Q., et al. Respiratory Research, 21: 154
Human neutralizing antibodies against SARS–CoV–2 require intact Fc effector functions for optimal therapeutic protection. (2021). Winkler, E., et al. Cell, 184(7): 1804-1820
Effect of Vaping on Lung Inflammation and SARS–CoV–2 Infection in a Hamster Model. (2022). Hinds, D., et al. ATS Journals
Determinants of SARS-CoV-2 entry and replication in airway mucosal tissue and susceptibility in smokers. (2021). Nakayama, T., et al. Cell Reports Medicine, 2(10)
Cigarette Smoke Regulates Endothelial ACE2 Expression in the Lung. (2022). Xing, D.D. et al. ATS Journals
and vitamin E acetate: Implications in the pathogenesis of EVALI but independent of SARS-COV-2 COVID-19 related proteins. (2020). Muthumalage, T., et al. Research Square
Chronic E-Cigarette Aerosol Inhalation Alters the Immune State of the Lungs and Increases ACE2 Expression, Raising Concern for Altered Response and Susceptibility to SARS-CoV-2. (2021). Masso-Silva, J.A. Frontiers in Physiology, https://doi.org/10.3389/fphys.2021.649604
Sex differences in the induction of angiotensin converting enzyme 2 (ACE-2) in mouse lungs after e-cigarette vapor exposure and its relevance to COVID-19. (2021). Naidu, V., et al. Journal of Investigative Medicine, 69(5)
Angiotensin-converting enzyme 2 expression in COPD and IPF fibroblasts: the forgotten cell in COVID-19. (2021). Aloufi, N., et al. Lung Cellular and Molecular Physiology, 320(1): 152-157
Mucus production stimulated by IFN-AhR signaling triggers hypoxia of COVID-19. (2020). Liu, Y., et al. Cell Research, 30: 1078-1087
Epithelial cell–specific loss of function of Miz1 causes a spontaneous COPD-like phenotype and up-regulates Ace2 expression in mice. (2020). Do-Umehara, H.C., et al. Science Advances, 6(33): DOI: 10.1126/sciadv.abb7238
Angiotensin-converting enzyme 2 expression in COPD and IPF fibroblasts: the forgotten cell in COVID-19. (2020). Aloufi, N., et al. American Journal of Physiology Lung Cell Molecular Physiology, 320(1): 152-157
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