Impaired inflammatory resolution with severe SARS-CoV-2 infection in leptin knock out obese hamster

Comorbidities, such as obesity, increase the risk of severe COVID-19. However, the mechanisms underlying severe illnesses in individuals with obesity are poorly understood. Here, we used gene-edited leptin knock out (Leptin−/−) obese hamsters to establish a severe infection model. This model exhibit...

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Published iniScience Vol. 28; no. 2; p. 111837
Main Authors Jiang, Ren-Di, Luo, Yun-Zhe, Lin, Hao-Feng, Zheng, Xiao-Shuang, Zeng, Wen-Tao, Liu, Mei-Qin, Deng, Hao-Hao, Wang, Qi, Lai, Ya-Na, Chen, Ying, Guo, Zi-Shuo, Zeng, Ya, Gong, Qian-Chun, Qiu, Chen, Dong, Mei, Wang, Xi, Wang, Zi-Yi, Ji, Li-Na, Hou, Pan-Pan, Li, Qian, Shen, Xu-Rui, Li, Bei, Gao, Yun, Zhang, Ai-Hua, Jiang, Ting-Ting, Shi, Ai-Min, Zhou, Peng, Lin, Xin-Hua, Deng, Zi-Qing, Li, Jian-Min, Shi, Zheng-Li
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 21.02.2025
Elsevier
Subjects
Immune response
Omics
Virology
Immune response
Omics
Virology
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Abstract Comorbidities, such as obesity, increase the risk of severe COVID-19. However, the mechanisms underlying severe illnesses in individuals with obesity are poorly understood. Here, we used gene-edited leptin knock out (Leptin−/−) obese hamsters to establish a severe infection model. This model exhibits robust viral replication, severe lung lesions, pronounced clinical symptoms, and fatal infection, mirroring severe COVID-19 in patients with obesity. Using single-cell transcriptomics on lung tissues pre- and post-infection, we found that monocyte-derived alveolar macrophages (MD-AM) play a key role in lung hyper-inflammation, including two unique MD-AM cell fate branches specific to Leptin−/− hamsters. Notably, reduced Trem2-dependent efferocytosis pathways in Leptin−/− hamsters indicated weakened inflammation resolution, consistent with the scRNA-seq data from patients with obesity. In summary, our study highlights the obesity-associated mechanisms underlying severe SARS-CoV-2 infections and establishes a reliable preclinical animal model for developing obesity-specific therapeutics for critical COVID-19. [Display omitted] •Leptin knock out obese hamsters were generated by using CRISPR/Cas9 technology•SARS-CoV-2 infection results in severe pneumonia and death in Leptin−/− obese hamsters•SARS-CoV-2 infection induces attenuated inflammatory resolution in Leptin−/− obese hamsters•Imbalanced Trem1/Trem2 in MD-AMs contribute to obesity-associated severe infection Immune response; Virology; Omics
AbstractList Comorbidities, such as obesity, increase the risk of severe COVID-19. However, the mechanisms underlying severe illnesses in individuals with obesity are poorly understood. Here, we used gene-edited leptin knock out (Leptin−/−) obese hamsters to establish a severe infection model. This model exhibits robust viral replication, severe lung lesions, pronounced clinical symptoms, and fatal infection, mirroring severe COVID-19 in patients with obesity. Using single-cell transcriptomics on lung tissues pre- and post-infection, we found that monocyte-derived alveolar macrophages (MD-AM) play a key role in lung hyper-inflammation, including two unique MD-AM cell fate branches specific to Leptin−/− hamsters. Notably, reduced Trem2-dependent efferocytosis pathways in Leptin−/− hamsters indicated weakened inflammation resolution, consistent with the scRNA-seq data from patients with obesity. In summary, our study highlights the obesity-associated mechanisms underlying severe SARS-CoV-2 infections and establishes a reliable preclinical animal model for developing obesity-specific therapeutics for critical COVID-19.
Comorbidities, such as obesity, increase the risk of severe COVID-19. However, the mechanisms underlying severe illnesses in individuals with obesity are poorly understood. Here, we used gene-edited leptin knock out (Leptin -/-) obese hamsters to establish a severe infection model. This model exhibits robust viral replication, severe lung lesions, pronounced clinical symptoms, and fatal infection, mirroring severe COVID-19 in patients with obesity. Using single-cell transcriptomics on lung tissues pre- and post-infection, we found that monocyte-derived alveolar macrophages (MD-AM) play a key role in lung hyper-inflammation, including two unique MD-AM cell fate branches specific to Leptin -/- hamsters. Notably, reduced Trem2-dependent efferocytosis pathways in Leptin -/- hamsters indicated weakened inflammation resolution, consistent with the scRNA-seq data from patients with obesity. In summary, our study highlights the obesity-associated mechanisms underlying severe SARS-CoV-2 infections and establishes a reliable preclinical animal model for developing obesity-specific therapeutics for critical COVID-19.Comorbidities, such as obesity, increase the risk of severe COVID-19. However, the mechanisms underlying severe illnesses in individuals with obesity are poorly understood. Here, we used gene-edited leptin knock out (Leptin -/-) obese hamsters to establish a severe infection model. This model exhibits robust viral replication, severe lung lesions, pronounced clinical symptoms, and fatal infection, mirroring severe COVID-19 in patients with obesity. Using single-cell transcriptomics on lung tissues pre- and post-infection, we found that monocyte-derived alveolar macrophages (MD-AM) play a key role in lung hyper-inflammation, including two unique MD-AM cell fate branches specific to Leptin -/- hamsters. Notably, reduced Trem2-dependent efferocytosis pathways in Leptin -/- hamsters indicated weakened inflammation resolution, consistent with the scRNA-seq data from patients with obesity. In summary, our study highlights the obesity-associated mechanisms underlying severe SARS-CoV-2 infections and establishes a reliable preclinical animal model for developing obesity-specific therapeutics for critical COVID-19.
Comorbidities, such as obesity, increase the risk of severe COVID-19. However, the mechanisms underlying severe illnesses in individuals with obesity are poorly understood. Here, we used gene-edited leptin knock out (Leptin−/−) obese hamsters to establish a severe infection model. This model exhibits robust viral replication, severe lung lesions, pronounced clinical symptoms, and fatal infection, mirroring severe COVID-19 in patients with obesity. Using single-cell transcriptomics on lung tissues pre- and post-infection, we found that monocyte-derived alveolar macrophages (MD-AM) play a key role in lung hyper-inflammation, including two unique MD-AM cell fate branches specific to Leptin−/− hamsters. Notably, reduced Trem2-dependent efferocytosis pathways in Leptin−/− hamsters indicated weakened inflammation resolution, consistent with the scRNA-seq data from patients with obesity. In summary, our study highlights the obesity-associated mechanisms underlying severe SARS-CoV-2 infections and establishes a reliable preclinical animal model for developing obesity-specific therapeutics for critical COVID-19. [Display omitted] •Leptin knock out obese hamsters were generated by using CRISPR/Cas9 technology•SARS-CoV-2 infection results in severe pneumonia and death in Leptin−/− obese hamsters•SARS-CoV-2 infection induces attenuated inflammatory resolution in Leptin−/− obese hamsters•Imbalanced Trem1/Trem2 in MD-AMs contribute to obesity-associated severe infection Immune response; Virology; Omics
Comorbidities, such as obesity, increase the risk of severe COVID-19. However, the mechanisms underlying severe illnesses in individuals with obesity are poorly understood. Here, we used gene-edited leptin knock out ( ) obese hamsters to establish a severe infection model. This model exhibits robust viral replication, severe lung lesions, pronounced clinical symptoms, and fatal infection, mirroring severe COVID-19 in patients with obesity. Using single-cell transcriptomics on lung tissues pre- and post-infection, we found that monocyte-derived alveolar macrophages (MD-AM) play a key role in lung hyper-inflammation, including two unique MD-AM cell fate branches specific to hamsters. Notably, reduced Trem2-dependent efferocytosis pathways in hamsters indicated weakened inflammation resolution, consistent with the scRNA-seq data from patients with obesity. In summary, our study highlights the obesity-associated mechanisms underlying severe SARS-CoV-2 infections and establishes a reliable preclinical animal model for developing obesity-specific therapeutics for critical COVID-19.
Comorbidities, such as obesity, increase the risk of severe COVID-19. However, the mechanisms underlying severe illnesses in individuals with obesity are poorly understood. Here, we used gene-edited leptin knock out ( Leptin −/− ) obese hamsters to establish a severe infection model. This model exhibits robust viral replication, severe lung lesions, pronounced clinical symptoms, and fatal infection, mirroring severe COVID-19 in patients with obesity. Using single-cell transcriptomics on lung tissues pre- and post-infection, we found that monocyte-derived alveolar macrophages (MD-AM) play a key role in lung hyper-inflammation, including two unique MD-AM cell fate branches specific to Leptin −/− hamsters. Notably, reduced Trem2-dependent efferocytosis pathways in Leptin −/− hamsters indicated weakened inflammation resolution, consistent with the scRNA-seq data from patients with obesity. In summary, our study highlights the obesity-associated mechanisms underlying severe SARS-CoV-2 infections and establishes a reliable preclinical animal model for developing obesity-specific therapeutics for critical COVID-19. • Leptin knock out obese hamsters were generated by using CRISPR/Cas9 technology • SARS-CoV-2 infection results in severe pneumonia and death in Leptin −/− obese hamsters • SARS-CoV-2 infection induces attenuated inflammatory resolution in Leptin −/− obese hamsters • Imbalanced Trem1/Trem2 in MD-AMs contribute to obesity-associated severe infection Immune response; Virology; Omics
ArticleNumber 111837
Author Shen, Xu-Rui
Deng, Hao-Hao
Chen, Ying
Lin, Xin-Hua
Zhou, Peng
Guo, Zi-Shuo
Liu, Mei-Qin
Zeng, Ya
Wang, Xi
Jiang, Ren-Di
Ji, Li-Na
Li, Jian-Min
Dong, Mei
Shi, Ai-Min
Zeng, Wen-Tao
Lai, Ya-Na
Gong, Qian-Chun
Wang, Zi-Yi
Jiang, Ting-Ting
Zheng, Xiao-Shuang
Shi, Zheng-Li
Qiu, Chen
Li, Qian
Zhang, Ai-Hua
Li, Bei
Wang, Qi
Luo, Yun-Zhe
Gao, Yun
Deng, Zi-Qing
Hou, Pan-Pan
Lin, Hao-Feng
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Virology
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Snippet Comorbidities, such as obesity, increase the risk of severe COVID-19. However, the mechanisms underlying severe illnesses in individuals with obesity are...
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SubjectTerms Immune response
Omics
Virology
Title Impaired inflammatory resolution with severe SARS-CoV-2 infection in leptin knock out obese hamster
URI https://dx.doi.org/10.1016/j.isci.2025.111837
https://www.ncbi.nlm.nih.gov/pubmed/39981511
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