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] |