Elovanoids downregulate SARS-CoV-2 cell-entry, canonical mediators and enhance protective signaling in human alveolar cells
| Autor: | Aram Asatryan, Pranab K. Mukherjee, Khanh Do, Surjyadipta Bhattacharjee, Marie-Audrey Ines Kautzmann, Nicolas G. Bazan, Jorgelina M. Calandria, Bokkyoo Jun, William C. Gordon, Nicholas J. Maness, Nicos A. Petasis |
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| Rok vydání: | 2021 |
| Předmět: |
Science
Cell SARS virus Antiviral Agents Article Virus Alveolar cells chemistry.chemical_compound Downregulation and upregulation Biosynthesis medicine Humans Cells Cultured chemistry.chemical_classification Multidisciplinary Lung SARS-CoV-2 Chemistry COVID-19 Lipid signaling Virus Internalization COVID-19 Drug Treatment Cell biology medicine.anatomical_structure Enzyme Alveolar Epithelial Cells Spike Glycoprotein Coronavirus Medicine Angiotensin-Converting Enzyme 2 Signal Transduction |
| Zdroj: | Scientific Reports, Vol 11, Iss 1, Pp 1-8 (2021) Scientific Reports |
| ISSN: | 2045-2322 |
| DOI: | 10.1038/s41598-021-91794-z |
| Popis: | The pro-homeostatic lipid mediators elovanoids (ELVs) attenuate cell binding and entrance of the SARS-CoV-2 receptor-binding domain (RBD) as well as of the SARS-CoV-2 virus in human primary alveoli cells in culture. We uncovered that very-long-chain polyunsaturated fatty acid precursors (VLC-PUFA, n-3) activate ELV biosynthesis in lung cells. Both ELVs and their precursors reduce the binding to RBD. ELVs downregulate angiotensin-converting enzyme 2 (ACE2) and enhance the expression of a set of protective proteins hindering cell surface virus binding and upregulating defensive proteins against lung damage. In addition, ELVs and their precursors decreased the signal of spike (S) protein found in SARS-CoV-2 infected cells, suggesting that the lipids curb viral infection. These findings open avenues for potential preventive and disease-modifiable therapeutic approaches for COVID-19. |
| Databáze: | OpenAIRE |
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