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Synergistic Role of NK Cells and Monocytes in Promoting Atherogenesis in Severe COVID-19 Patients
Insights
Severe COVID-19 infection increases cardiovascular disease risk. Proinflammatory monocytes and activated Natural Killer (NK) cells synergistically drive atherogenesis by promoting oxidized LDL uptake and foam cell formation post-infection.
Area of Science:
- Immunology
- Cardiovascular Science
- Infectious Disease
Background:
- Severe COVID-19 is linked to increased cardiovascular disease (CVD) risk, potentially due to immune dysregulation.
- Monocytes, macrophages, and Natural Killer (NK) cells are implicated in atherosclerosis and are known to be altered during severe COVID-19.
Approach:
- Investigated the synergistic roles of monocytes and NK cells in atherogenesis following severe COVID-19.
- Analyzed immune cell phenotypes and their interactions with vascular tissue and oxidized low-density lipoprotein (Ox-LDL).
Key Points:
- Circulating proinflammatory monocytes and activated NK cells synergistically promote Ox-LDL uptake in vascular tissue post-severe COVID-19.
- This interaction leads to foam cell generation and contributes to atherogenesis, even after recovery from acute infection.
- Altered immune cell phenotypes play a critical role in COVID-19-associated atherogenesis.
Conclusions:
- Monocytes/macrophages and NK cells are key players in the development of atherosclerosis after severe COVID-19.
- These findings offer new insights into the mechanisms linking severe viral infections to long-term cardiovascular complications.
Abstract:
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.
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