期刊
VIRUSES-BASEL
卷 13, 期 4, 页码 -出版社
MDPI
DOI: 10.3390/v13040639
关键词
vasculitis; vasculopathy; SARS-CoV-2; COVID-19; aquaporin 1; hamster; perivascular edema; endothelium
类别
资金
- Covid-19 Rapid Response Grant of the German Ministry of Health (BMG)
- BMBF (Federal Ministry of Education and Research) project entitled RAPID (Risk assessment in re-pandemic respiratory infectious diseases) [01KI1723G]
- Ministry of Science and Culture of Lower Saxony in Germany [14-76103-184 CORONA-15/20]
- German Research Foundation (Deutsche Forschungsgemeinschaft) [406109949]
- Deutsche Forschungsgemeinschaft
- University of Veterinary Medicine Hannover, Foundation
The study found that SARS-CoV-2 infection causes endothelial hypertrophy, endothelialitis, and vasculitis, with inflammation mainly consisting of macrophages and fewer T-lymphocytes and neutrophils/heterophils infiltrating vascular walls. Affected vessels exhibit edema formation associated with loss of aquaporin 1 on endothelial cells.
Vascular changes represent a characteristic feature of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection leading to a breakdown of the vascular barrier and subsequent edema formation. The aim of this study was to provide a detailed characterization of the vascular alterations during SARS-CoV-2 infection and to evaluate the impaired vascular integrity. Groups of ten golden Syrian hamsters were infected intranasally with SARS-CoV-2 or phosphate-buffered saline (mock infection). Necropsies were performed at 1, 3, 6, and 14 days post-infection (dpi). Lung samples were investigated using hematoxylin and eosin, alcian blue, immunohistochemistry targeting aquaporin 1, CD3, CD204, CD31, laminin, myeloperoxidase, SARS-CoV-2 nucleoprotein, and transmission electron microscopy. SARS-CoV-2 infected animals showed endothelial hypertrophy, endothelialitis, and vasculitis. Inflammation mainly consisted of macrophages and lower numbers of T-lymphocytes and neutrophils/heterophils infiltrating the vascular walls as well as the perivascular region at 3 and 6 dpi. Affected vessels showed edema formation in association with loss of aquaporin 1 on endothelial cells. In addition, an ultrastructural investigation revealed disruption of the endothelium. Summarized, the presented findings indicate that loss of aquaporin 1 entails the loss of intercellular junctions resulting in paracellular leakage of edema as a key pathogenic mechanism in SARS-CoV-2 triggered pulmonary lesions.
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