tetano
Editor, Senior Moderator
Cell Rep
. 2024 Jun 10;43(6):114328.
doi: 10.1016/j.celrep.2024.114328. Online ahead of print. Single-cell-resolved interspecies comparison shows a shared inflammatory axis and a dominant neutrophil-endothelial program in severe COVID-19
Stefan Peidli[SUP] 1 [/SUP], Geraldine Nouailles[SUP] 2 [/SUP], Emanuel Wyler[SUP] 3 [/SUP], Julia M Adler[SUP] 4 [/SUP], Sandra Kunder[SUP] 5 [/SUP], Anne Voß[SUP] 5 [/SUP], Julia Kazmierski[SUP] 6 [/SUP], Fabian Pott[SUP] 6 [/SUP], Peter Pennitz[SUP] 2 [/SUP], Dylan Postmus[SUP] 6 [/SUP], Luiz Gustavo Teixeira Alves[SUP] 3 [/SUP], Christine Goffinet[SUP] 6 [/SUP], Achim D Gruber[SUP] 5 [/SUP], Nils Blüthgen[SUP] 1 [/SUP], Martin Witzenrath[SUP] 7 [/SUP], Jakob Trimpert[SUP] 8 [/SUP], Markus Landthaler[SUP] 9 [/SUP], Samantha D Praktiknjo[SUP] 10 [/SUP]
Affiliations
A key issue for research on COVID-19 pathogenesis is the lack of biopsies from patients and of samples at the onset of infection. To overcome these hurdles, hamsters were shown to be useful models for studying this disease. Here, we further leverage the model to molecularly survey the disease progression from time-resolved single-cell RNA sequencing data collected from healthy and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-infected Syrian and Roborovski hamster lungs. We compare our data to human COVID-19 studies, including bronchoalveolar lavage, nasal swab, and postmortem lung tissue, and identify a shared axis of inflammation dominated by macrophages, neutrophils, and endothelial cells, which we show to be transient in Syrian and terminal in Roborovski hamsters. Our data suggest that, following SARS-CoV-2 infection, commitment to a type 1- or type 3-biased immunity determines moderate versus severe COVID-19 outcomes, respectively.
Keywords: COVID-19; CP: Immunology; CP: Microbiology; SARS-CoV-2; computational biology; endothelial cells; innate immunity; lungs; machine learning; neutrophils; pathogenesis; single-cell.
. 2024 Jun 10;43(6):114328.
doi: 10.1016/j.celrep.2024.114328. Online ahead of print. Single-cell-resolved interspecies comparison shows a shared inflammatory axis and a dominant neutrophil-endothelial program in severe COVID-19
Stefan Peidli[SUP] 1 [/SUP], Geraldine Nouailles[SUP] 2 [/SUP], Emanuel Wyler[SUP] 3 [/SUP], Julia M Adler[SUP] 4 [/SUP], Sandra Kunder[SUP] 5 [/SUP], Anne Voß[SUP] 5 [/SUP], Julia Kazmierski[SUP] 6 [/SUP], Fabian Pott[SUP] 6 [/SUP], Peter Pennitz[SUP] 2 [/SUP], Dylan Postmus[SUP] 6 [/SUP], Luiz Gustavo Teixeira Alves[SUP] 3 [/SUP], Christine Goffinet[SUP] 6 [/SUP], Achim D Gruber[SUP] 5 [/SUP], Nils Blüthgen[SUP] 1 [/SUP], Martin Witzenrath[SUP] 7 [/SUP], Jakob Trimpert[SUP] 8 [/SUP], Markus Landthaler[SUP] 9 [/SUP], Samantha D Praktiknjo[SUP] 10 [/SUP]
Affiliations
- PMID: 38861386
- DOI: 10.1016/j.celrep.2024.114328
A key issue for research on COVID-19 pathogenesis is the lack of biopsies from patients and of samples at the onset of infection. To overcome these hurdles, hamsters were shown to be useful models for studying this disease. Here, we further leverage the model to molecularly survey the disease progression from time-resolved single-cell RNA sequencing data collected from healthy and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)-infected Syrian and Roborovski hamster lungs. We compare our data to human COVID-19 studies, including bronchoalveolar lavage, nasal swab, and postmortem lung tissue, and identify a shared axis of inflammation dominated by macrophages, neutrophils, and endothelial cells, which we show to be transient in Syrian and terminal in Roborovski hamsters. Our data suggest that, following SARS-CoV-2 infection, commitment to a type 1- or type 3-biased immunity determines moderate versus severe COVID-19 outcomes, respectively.
Keywords: COVID-19; CP: Immunology; CP: Microbiology; SARS-CoV-2; computational biology; endothelial cells; innate immunity; lungs; machine learning; neutrophils; pathogenesis; single-cell.