Abstract
An array of infections, including the novel coronavirus (SARS-CoV-2), trigger macrophage activation syndrome (MAS) and subsequently hypercytokinemia, commonly referred to as a cytokine storm (CS). It is postulated that CS is mainly responsible for critical COVID-19 cases, including acute respiratory distress syndrome (ARDS). Recognizing the therapeutic potential of Spirulina blue-green algae (Arthrospira platensis), in this in vitro stimulation study, LPS-activated macrophages and monocytes were treated with aqueous extracts of Spirulina, cultivated in either natural or controlled light conditions. We report that an extract of photosynthetically controlled Spirulina (LED Spirulina), at a concentration of 0.1 µg/mL, decreases macrophage and monocyte-induced TNF-α secretion levels by over 70% and 40%, respectively. We propose prompt in vivo studies in animal models and human subjects to determine the putative effectiveness of a natural, algae-based treatment for viral CS and ARDS, and explore the potential of a novel anti-TNF-α therapy.Graphical abstract
Highlights
The novel coronavirus disease (COVID-19) is an emerging contagious respiratory tract illness caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) (Hu et al 2020)
We report that an aqueous extract of a photosynthetically controlled Spirulina (LED Spirulina) inhibits tumor necrosis factor (TNF)-α secretion by over 70% from LPS-activated macrophages and over 40% from LPS-activated monocyte cells
As reported in previous studies (Feldmann et al 2020), critically ill COVID-19 patients who were administered a single dose of a TNF- neutralizing antibody were 45% less likely to die overall, and more likely to be weaning from mechanical ventilation 1 month after treatment, compared with untreated patients
Summary
The novel coronavirus disease (COVID-19) is an emerging contagious respiratory tract illness caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) (Hu et al 2020). Epidemiological studies have indicated that exposure to the etiologic agent SARS-CoV-2 provokes macrophages and monocytes to release an excessive amount of different pro-inflammatory cytokines, such as tumor necrosis factor (TNF)-α and interleukin (IL)-6, to cause a hypercytokinemia, commonly referred to as a cytokine storm (CS) (Ishikawa 2012; Ye et al 2020). A recent analysis indicated higher systemic levels of IL-2, IL-7, IL-10, monocyte chemoattractant protein-1 (MCP1), macrophage inflammatory protein-1A (MIP-1A), and TNF-α, among critically ill COVID-19 patients (McGonagle et al 2020; Ruan et al 2020). Excess release of TNF-α plays a critical role in disrupting the lung endothelial and epithelial barriers, which may cause acute respiratory distress
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