Table 1.
Effect | Mechanism | Reference |
---|---|---|
Inactivates viruses | Induction of cathelicidin | [47] |
Reduces risk of cytokine storm | Reduces concentration of proinflammatory cytokines and increases concentration of anti-inflammatory cytokines | [24] |
Reduces risk of cytokine storm | Induces T regulatory cell production | [27] |
Reduces risk of pneumonia | Reduces risk of endothelial dysfunction | [48] |
Increases the metabolic tolerance of the host to damage inflicted by the pathogen infection | Reduces matrix metalloproteinase-9 concentrations | [49] |
Reduces free SARS-CoV-2 concentrations | Increases soluble ACE2 concentrations that can bind to SARS-CoV-2 | [50] |
Anti-viral effects | Balanced differentiation of effector CD8 and CD4 T cells | [51] |
Reduces risk of myocarditis | Reduces concentration of catecholamines | [52] |
Reduces risk of myocarditis | Inhibits RAS | [53] |
Reduces risk of vascular dilation and permeability and hypotensin | Inhibits RAS-mediated bradykinin storm | [46] |
Protects against the effects of histamines such as acute immune-mediated reactions [54], lung dysregulation [55], increase in Th2 and decrease in Th1 cytokines [56], and thus susceptibility to respiratory tract infections [57] | Preserves stability of mast cells, which can release histamine when activated. | [58] |
Promotes adaptive immunity | Regulations of T cell proliferation | [27] |
Neuroprotection | Reduces inflammation and oxidative stress | [59] |
Protection against exacerbation by other viruses | Reduces risk of Epstein–Barr virus infection | [60] |
Abbreviations: SARS-CoV-2 = severe acute respiratory syndrome coronavirus 2; ACE2 = angiotensin-converting enzyme 2; RAS = renin angiotensin system.