Immunometabolic Mechanisms Underlying the Severity of COVID-19

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Editorial

20 July 2022

Editorial: Immunometabolic mechanisms underlying the severity of COVID-19

Julia Kzhyshkowska

,

Vishwanath Venketaraman

and

Galileo Escobedo

2,555 views

2 citations

Editors

3

Galileo Escobedo

General Hospital of Mexico

Vishwanath Venketaraman

Western University of Health Sciences

Julia Kzhyshkowska

Heidelberg University

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The novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causal agent of the global outbreak of coronavirus disease 2019 (COVID-19). An important number of patients with COVID-19 are at higher risk of developing the most severe form of the disease that includes pneumonia, acute respiratory distress syndrome (ARDS), multiorgan failure, and death. Fatal cases of COVID-19 are more prevalent in patients with preexisting comorbidities such as obesity, hypertension, and type 2 diabetes (T2D). These patients also experience a cytokine storm characterized by increased levels of proinflammatory cytokines such as interleukin (IL-) 1 beta, IL-6, and tumor necrosis factor alpha (TNF-alpha), among others. However, the mechanisms by which comorbidities contribute to the cytokine storm, increasing the progression, severity, and mortality of COVID-19 are not yet fully understood. Metabolic and cardiovascular comorbidities are characterized by the presence of immunometabolic agents such as excess glucose, free-fatty acids (FFA), low-density lipoproteins (LDL), and uric acid that appear to act in synergy with immune cells to promote the inflammatory response through mechanisms still unknown in COVID-19.

The main goal of this Research Topic is to congregate eminent contributors in the fields of metabolic and cardiovascular diseases, immune responses, and COVID-19, whose work helps elucidate the mechanisms of the cross-talk between the metabolic and immunological pathways that have essential effects on the adaptive and innate immune responses, including T cell exhaustion, antibody deficiency, cytokine storm, complement activity and neutrophil trafficking in patients with preexisting comorbidities experiencing COVID-19. Furthermore, we invite submissions that characterize the cell signaling pathways that mediate the effect of excess glucose, FFA, LDL, uric acid, and insulin, among others on T and B lymphocytes, monocytes and macrophages, neutrophils, and basophils in patients with SARS-CoV-2 infection.

In this Research Topic we welcome the submission of Original Research (basic and clinical studies as well Clinical Trials) and Review articles addressing in vitro and in vivo studies focused on these potential topics, but not limited to:

1. Role of excess glucose, FFA, LDL, uric acid, and insulin, among others in immune cell activation and cytokine release in patients with SARS-CoV-2 infection.

2. Effect of immunometabolic agents on chemokine production and neutrophil infiltration into airway epithelium, vascular endothelium, and pancreas of patients with COVID-19.

3. Profiling of immune cell subpopulations in COVID-19 patients with cardio-metabolic disorders.

4. Contribution of obesity, hypertension, T2D, insulin resistance, dyslipidemia, and metabolic syndrome to vascular inflammation in patients with SARS-CoV-2 infection

5. Characterization of cell signaling pathways mediating the effect of immunometabolic agents on immune cell activity in SARS-CoV-2 infection.

6. Therapeutic targets based on inhibiting the action of immunometabolic agents in COVID-19.