tetano
Editor, Senior Moderator
Viruses
. 2021 Apr 8;13(4):639.
doi: 10.3390/v13040639.
Vascular Inflammation Is Associated with Loss of Aquaporin 1 Expression on Endothelial Cells and Increased Fluid Leakage in SARS-CoV-2 Infected Golden Syrian Hamsters
Lisa Allnoch[SUP] 1 [/SUP], Georg Beythien[SUP] 1 [/SUP], Eva Leitzen[SUP] 1 [/SUP], Kathrin Becker[SUP] 1 [/SUP], Franz-Josef Kaup[SUP] 1 [/SUP], Stephanie Stanelle-Bertram[SUP] 2 [/SUP], Berfin Schaumburg[SUP] 2 [/SUP], Nancy Mounogou Kouassi[SUP] 2 [/SUP], Sebastian Beck[SUP] 2 [/SUP], Martin Zickler[SUP] 2 [/SUP], Vanessa Herder[SUP] 1 [/SUP], G?lsah Gabriel[SUP] 2 3 [/SUP], Wolfgang Baumg?rtner[SUP] 1 [/SUP]
Affiliations
Abstract
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.
Keywords: COVID-19; SARS-CoV-2; aquaporin 1; endothelium; hamster; perivascular edema; vasculitis; vasculopathy.
. 2021 Apr 8;13(4):639.
doi: 10.3390/v13040639.
Vascular Inflammation Is Associated with Loss of Aquaporin 1 Expression on Endothelial Cells and Increased Fluid Leakage in SARS-CoV-2 Infected Golden Syrian Hamsters
Lisa Allnoch[SUP] 1 [/SUP], Georg Beythien[SUP] 1 [/SUP], Eva Leitzen[SUP] 1 [/SUP], Kathrin Becker[SUP] 1 [/SUP], Franz-Josef Kaup[SUP] 1 [/SUP], Stephanie Stanelle-Bertram[SUP] 2 [/SUP], Berfin Schaumburg[SUP] 2 [/SUP], Nancy Mounogou Kouassi[SUP] 2 [/SUP], Sebastian Beck[SUP] 2 [/SUP], Martin Zickler[SUP] 2 [/SUP], Vanessa Herder[SUP] 1 [/SUP], G?lsah Gabriel[SUP] 2 3 [/SUP], Wolfgang Baumg?rtner[SUP] 1 [/SUP]
Affiliations
- PMID: 33918079
- DOI: 10.3390/v13040639
Abstract
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.
Keywords: COVID-19; SARS-CoV-2; aquaporin 1; endothelium; hamster; perivascular edema; vasculitis; vasculopathy.