The following is the summary of “Steen solution protects pulmonary microvascular endothelial cells and preserves endothelial barrier after lipopolysaccharide-induced injury” published in the January 2023 issue of Thoracic and cardiovascular surgery by Ta, et al.
The severe outcome of acute lung injury is acute respiratory distress syndrome, which carries a high fatality rate. Acute respiratory distress syndrome is a life-threatening condition, but there are only a few ways to help the lungs recover. The normothermic ex vivo and in vivo perfusion with Steen solution has been shown to be effective in our lab for rehabilitating sepsis-injured lungs (Steen). In spite of this, the mechanisms by which Steen exerts its protective benefits still need to be better understood. Here, researchers investigate if Steen mitigates the lipopolysaccharide-induced breakdown of the pulmonary endothelial barrier and the subsequent inflammation it causes.
After exposure to lipopolysaccharide for 4 hours, primary pulmonary microvascular endothelial cells were cultured in complete media (Media), Steen, or Steen followed by complete media (Steen/Media) for 8 hours to recover. Endothelial cells in the pulmonary microvasculature were tested in accordance with established protocols to determine levels of oxidative stress, chemokines, permeability, interendothelial junction proteins, and toll-like receptor 4-mediated pathways. Pulmonary microvascular endothelial cells treated with lipopolysaccharide and then allowed to recover in Media showed significant increases in reactive oxygen species, lipid peroxidation, expression of chemokines (such as chemokine [C-X-C motif] ligand 1 and chemokine [C-C motif] ligand 2) and cell adhesion molecules (P-selectin, E-selectin, and vascular cell adhesion molecule 1) (zonula occludens-1, zonula occludens-2, and vascular endothelial-cadherin).
The inflammatory pathways were greatly reduced when pulmonary microvascular endothelial cells were restored in either Steen or Steen/Media. After LPS exposure, Steen solution protects pulmonary endothelial barrier function by fostering an anti-inflammatory environment by suppressing oxidative stress, toll-like receptor 4-mediated signaling, and preservation of interendothelial junctions. These defense mechanisms shed light on how to better use in vivo lung perfusion with Steen to treat severe cases of acute respiratory distress syndrome.
Source: sciencedirect.com/science/article/pii/S0022522322004093
