tetano
Editor, Senior Moderator
J Vis Exp
. 2026 Sep 11
235).
doi: 10.3791/72297.
Ke Liu # 1 , Huiping Yang # 2 , Wei Zheng # 2 , Kexin Yu 1 , Yi Zhu 1 , Yufei Liu 1 , Yi Zeng 1 , Keliang Liu 3 , Chuantao Zhang 4
Affiliations Expand
Despite the widespread implementation of vaccination and antiviral therapies, SARS-CoV-2 infection continues to cause substantial morbidity and mortality among vulnerable populations, underscoring the urgent need for reliable experimental models to investigate the pathogenesis of COVID-19, elucidate the mechanisms of drug action, and evaluate potential therapeutic strategies. SARS-CoV-2 infection can cause severe lung injury, characterized by excessive inflammatory responses and impaired type I interferon (IFN-I)-mediated antiviral immunity; however, current animal models remain limited in recapitulating the dysregulated immune-inflammatory responses associated with COVID-19. A SARS-CoV-2 and LPS-induced mouse model of COVID-19-associated lung injury was developed to recapitulate key immunopathological features of COVID-19. This model induces prominent pathological features in lung tissue, including inflammatory cell infiltration, alveolar structural destruction, and elevated expression of pro-inflammatory cytokines, accompanied by impaired IFN-I responses. This study provides a detailed description of the procedures used to establish the SARS-CoV-2 and LPS-induced mouse model of lung injury and systematically characterizes the model through analyses of lung histopathological alterations, viral load, inflammatory cytokines, and IFN-I levels. This model offers an experimental platform for investigating the immune-inflammatory mechanisms underlying COVID-19-associated lung injury and the processes involved in lung tissue repair, while also providing a foundation for evaluating therapeutic strategies aimed at alleviating immune-inflammatory dysregulation and promoting recovery of pulmonary function.
. 2026 Sep 11
235).doi: 10.3791/72297.
A Mouse Model of Coronavirus Disease 2019-Associated Lung Injury Induced by Severe Acute Respiratory Syndrome Coronavirus 2 and Lipopolysaccharide
Ke Liu # 1 , Huiping Yang # 2 , Wei Zheng # 2 , Kexin Yu 1 , Yi Zhu 1 , Yufei Liu 1 , Yi Zeng 1 , Keliang Liu 3 , Chuantao Zhang 4
Affiliations Expand
- PMID: 42730669
- DOI: 10.3791/72297
Abstract
Despite the widespread implementation of vaccination and antiviral therapies, SARS-CoV-2 infection continues to cause substantial morbidity and mortality among vulnerable populations, underscoring the urgent need for reliable experimental models to investigate the pathogenesis of COVID-19, elucidate the mechanisms of drug action, and evaluate potential therapeutic strategies. SARS-CoV-2 infection can cause severe lung injury, characterized by excessive inflammatory responses and impaired type I interferon (IFN-I)-mediated antiviral immunity; however, current animal models remain limited in recapitulating the dysregulated immune-inflammatory responses associated with COVID-19. A SARS-CoV-2 and LPS-induced mouse model of COVID-19-associated lung injury was developed to recapitulate key immunopathological features of COVID-19. This model induces prominent pathological features in lung tissue, including inflammatory cell infiltration, alveolar structural destruction, and elevated expression of pro-inflammatory cytokines, accompanied by impaired IFN-I responses. This study provides a detailed description of the procedures used to establish the SARS-CoV-2 and LPS-induced mouse model of lung injury and systematically characterizes the model through analyses of lung histopathological alterations, viral load, inflammatory cytokines, and IFN-I levels. This model offers an experimental platform for investigating the immune-inflammatory mechanisms underlying COVID-19-associated lung injury and the processes involved in lung tissue repair, while also providing a foundation for evaluating therapeutic strategies aimed at alleviating immune-inflammatory dysregulation and promoting recovery of pulmonary function.