| Autor: |
Gunasena M, Alles M, Wijewantha Y, Mulhern W, Bowman E, Gabriel J, Kettelhut A, Kumar A, Weragalaarachchi K, Kasturiratna D, Horowitz JC, Scrape S, Pannu SR, Liu SL, Vilgelm A, Wijeratne S, Bednash JS, Demberg T, Funderburg NT, Liyanage NPM |
| Jazyk: |
angličtina |
| Zdroj: |
MedRxiv : the preprint server for health sciences [medRxiv] 2023 Nov 12. Date of Electronic Publication: 2023 Nov 12. |
| DOI: |
10.1101/2023.11.10.23298322 |
| Abstrakt: |
Clinical data demonstrate an increased predisposition to cardiovascular disease (CVD) following severe COVID-19 infection. This may be driven by a dysregulated immune response associated with severe disease. Monocytes and vascular tissue resident macrophages play a critical role in atherosclerosis, the main pathology leading to ischemic CVD. Natural killer (NK) cells are a heterogenous group of cells that are critical during viral pathogenesis and are known to be dysregulated during severe COVID-19 infection. Their role in atherosclerotic cardiovascular disease has recently been described. However, the contribution of their altered phenotypes to atherogenesis following severe COVID-19 infection is unknown. We demonstrate for the first time that during and after severe COVID-19, circulating proinflammatory monocytes and activated NK cells act synergistically to increase uptake of oxidized low-density lipoprotein (Ox-LDL) into vascular tissue with subsequent foam cell generation leading to atherogenesis despite recovery from acute infection. Our data provide new insights, revealing the roles of monocytes/macrophages, and NK cells in COVID-19-related atherogenesis. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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