Conclusions
We conclude that simple targeting strategies can mimic glycocalyx function under inflammatory conditions, effectively reducing neutrophil recruitment.
Methods
In this study, we examine the targeting of E-selectin by an engineered peptide moiety bound to a dermatan sulfate backbone. We further investigate this conjugate, denoted as EC-SEAL, by observing its binding to inflamed endothelium, and quantifying its ability to modulate neutrophil-endothelium interactions.
Results
Binding data reveal that EC-SEAL recognizes domains on E-selectin, and to a lesser degree on P- and L-selectin, and ICAM-1. Further, EC-SEAL increases neutrophil rolling velocity, and decreases neutrophil arrest and migration on inflamed human microvascular endothelial cells under physiologically relevant flow conditions. Conclusions: We conclude that simple targeting strategies can mimic glycocalyx function under inflammatory conditions, effectively reducing neutrophil recruitment.