Neutrophil adhesion to vessel walls impairs pulmonary circulation in COVID-19 pathology

Hiroshi Ueki (), I-Hsuan Wang, Maki Kiso, Kenta Horie, Shun Iida, Sohtaro Mine, Michiko Ujie, Hung-Wei Hsu, Chen-Hui Henry Wu, Masaki Imai, Tadaki Suzuki, Wataru Kamitani, Eiryo Kawakami and Yoshihiro Kawaoka ()
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Hiroshi Ueki: University of Tokyo
I-Hsuan Wang: Academia Sinica
Maki Kiso: University of Tokyo
Kenta Horie: Chiba University
Shun Iida: National Institute of Infectious Diseases
Sohtaro Mine: National Institute of Infectious Diseases
Michiko Ujie: University of Tokyo
Hung-Wei Hsu: Academia Sinica
Chen-Hui Henry Wu: Academia Sinica
Masaki Imai: University of Tokyo
Tadaki Suzuki: National Institute of Infectious Diseases
Wataru Kamitani: Gunma University Graduate School of Medicine
Eiryo Kawakami: Chiba University
Yoshihiro Kawaoka: University of Tokyo

Nature Communications, 2025, vol. 16, issue 1, 1-17

Abstract: Abstract Microthrombus formation is associated with COVID-19 severity; however, the detailed mechanism remains unclear. In this study, we investigated mouse models with severe pneumonia caused by SARS-CoV-2 infection by using our in vivo two-photon imaging system. In the lungs of SARS-CoV-2-infected mice, increased expression of adhesion molecules in intravascular neutrophils prolonged adhesion time to the vessel wall, resulting in platelet aggregation and impaired lung perfusion. Re-analysis of scRNA-seq data from peripheral blood mononuclear cells from COVID-19 cases revealed increased expression levels of CD44 and SELL in neutrophils in severe COVID-19 cases compared to a healthy group, consistent with our observations in the mouse model. These findings suggest that pulmonary perfusion defects caused by neutrophil adhesion to pulmonary vessels contribute to COVID-19 severity.

Date: 2025
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DOI: 10.1038/s41467-024-55272-0

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