Activation of Renin Angiotensin Aldosterone System (RAAS), leads to an increase of aldosterone levels in COVID-19 patients which may be associated with increased mortality due to cardiac arrest in COVID-19 infected patients. Aldosterone regulates the innate and adaptive immune response by promoting the activation of inflammatory mediators and cells such as monocytes, macrophages, dendritic cells (DCs), and lymphocytes.
The activation of these cells leads to cytokine storm, which correlates with the high mortality and sudden death in COVID-19 geriatric patients. Moreover, aldosterone aggravates the activity of DCs (dendritic cells) in SARS-CoV-2 infection. In vivo, DCs pre-treated with aldosterone show an increased capacity to activate CD 8+ T cells response and enhance Th 17 polarization of CD 4+ T cells. Additionally, this hormone can reduce regulatory T cells (T-reg) that in physiological conditions act as important immune suppressors and can lead to a reduction of vascular damages induced by aldosterone. Furthermore, decrease and dysregulation of T-reg have been suggested in COVID-19 infection, especially in older hospitalized patients.
Finally, concluding that in COVID-19 older patients, aldosterone may downregulate T-reg number, promoting vascular injury. This, in turn, enhances dendritic cells (DCs) function and induces a hyper-inflammatory state. This mechanism could be used for the development of new DC vaccines against COVID-19 with more effectiveness mostly in older patients with a poor antibody response to the vaccines currently. Further studies are necessary to evaluate in vivo and in vitro effects of aldosterone on SARS-CoV-2 affected cells and to test the potential beneficial effects of mineralocorticoid receptor antagonists (MRAs) in COVID-19 and the related cardiac complications.
Ref Link: Pubmed
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