Selectins and neutrophil elastase

Selectins and neutrophil elastase represent two distinct but functionally linked components of the inflammatory cascade, particularly in the context of leukocyte recruitment and tissue damage. Selectins (E, L, and P) are cell surface glycoproteins that mediate the initial rolling of neutrophils and other leukocytes on the vascular endothelium, which is a prerequisite for firm adhesion and extravasation into inflamed tissues. Once neutrophils reach the site of inflammation, they release neutrophil elastase, a potent serine protease capable of degrading various extracellular matrix components such as elastin and collagen, as well as activating other pro-inflammatory mediators. Therapeutic strategies targeting this axis aim to both prevent the influx of inflammatory cells and mitigate the subsequent proteolytic damage they cause. This dual-pronged approach is primarily investigated for chronic inflammatory conditions of the lung, such as chronic obstructive pulmonary disease (COPD) and cystic fibrosis, where excessive neutrophil activity is a hallmark of disease progression.

Other names

E-selectin (SELE)L-selectin (SELL)P-selectin (SELP)Neutrophil elastase (ELANE)Human neutrophil elastase (HNE)CD62ECD62LCD62PLeukocyte elastase

Inhibition of selectin-mediated leukocyte rolling and adhesion to the endothelium, combined with the inhibition of neutrophil elastase-mediated extracellular matrix degradation and pro-inflammatory signaling.