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Table 2 Role of non-immune soluble mediators in COVID-19 infection

From: Immune system-related soluble mediators and COVID-19: basic mechanisms and clinical perspectives

Soluble mediator

Biological role in COVID-19 infection

Output effect

References

sFlt-1

Excess level of sFlt-1 induce endothelial dysfunction and is associated with bacterial sepsis

Increase in SARS-CoV-2 infection and is correlated with disease severity, endothelial dysfunction and respiratory failure

Adverse effect

[64,65,66,67,68,69]

sACE2

Increase in viral infections like SARS-CoV-2

Interact with spike of SARS-CoV-2 and facilitate viral intery to the host

Increased sACE2 has correlation with inflammatory response and endothelial dysfunction

Controversial

[70, 72, 73]

sRAGE

Is associated with inflammatory diseases, bacterial infection, and lung damage

Diagnosis factor for ARDS

Adverse effect

[76,77,78]

suPAR

Is involved in plasminogen activation pathway, regulation of cell adhesion, and proliferation and migration by interacting with extracellular matrix proteins

Increased in infection and inflammatory conditions like arthritis, HIV infection

Cause immune response activation

Level of suPAR has positive correlation with severity and mortality of HIV and SARS-CoV-2

Adverse effect

[86,87,88,89]

  1. sFlt-1, soluble fms-like tyrosine kinase-1; sACE2, soluble angiotensin-converting enzyme 2; sRAGE, soluble receptor for advanced glycation end products; suPAR, soluble urokinase-type plasminogen activator receptor; HIV, human immune-deficiency virus; ARDS, acute respiratory distress syndrome