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Table 1 Ex vivo and in vitro immunomodulatory and barrier function effects of LMWF5A

From: The novel immunomodulatory biologic LMWF5A for pharmacological attenuation of the “cytokine storm” in COVID-19 patients: a hypothesis

Cell Model

Results

Conclusions

Study

Influenza HA presented human T-cell clone

LMWF5A and DA-DKP treatment results in:

↓ TNFα

↓ IFNγ

Reduced release of cytokines associated with COVID-19 cytokine storm.

[17]

Influenza HA presented and CD3/CD28 stimulated human T-cell clone

DA-DKP treatment results in:

↓ TNFα

↓ IFNγ

↑ RAP-1 phosphorylation and activity

Reduced release of cytokines associated with COVID-19 cytokine storm. Also, increased activation of barrier enhancing GTPase.

[18]

LPS-stimulated human PBMC

LMWF5A and DA-DKP treatment results in:

↓ TNFα

Reduced release of cytokine associated with COVID-19 cytokine storm.

[19]

LPS-stimulated human PBMC

LMWF5A treatment results in:

↓ TNFα

↑ PGE2 and 15d-PGJ2

Reduced release of cytokine associated with COVID-19 cytokine storm together with increased pro-resolving mediator release.

[20]

LPS-stimulated, PMA-differentiated THP-1 macrophages

LMWF5A treatment results in:

↓ IL-6, IL-12, and CXCL10

↑ IL-10

↑ AhR activity

Reduced release of cytokines associated with COVID-19 cytokine storm with apparent shift from M1 to M2 phenotype.

[21]

Monolayer and 3D cultured human BMMSC

LMWF5A treatment results in:

↓ RhoA activity

↑ Rac1 activity

↓ Stress fiber formation

↑ Stem cell homing potential

Rebalancing of overall GTPase activity conducive to barrier enhancement. Also, increased progenitor cell homing potential.

[22]

Dedifferentiated primary human chondrocytes

LMWF5A treatment results in:

↑ SRY-Box transcription factor

↓ Apoptosis

Activation of transcription factor protective of fibrosis and increased cell survival.

[23]

Primary human endothelial cell permeability models

LMWF5A treatment results in:

↑ Acetylation of α-tubulin

↓ Vascular leakage

Enhanced barrier function of endothelial cells with reduced vascular leakage. Also, apparent stabilization of microtubule network.

[24]