The Model of Neutrophil Chemotaxis Participated by the Vascular Endothelial Glycocalyx.

Abstract

The vascular endothelial glycocalyx is a critical structural and functional component. It maintains endothelial integrity, orchestrates hemodynamic regulation, enables selective blood component filtration, and mediates mechanotransduction. Existing in a dynamic equilibrium, this glycoprotein-polysaccharide matrix provides an interactive platform for intravascular reactions and actively participates in innate immune responses (eg, neutrophil chemotaxis and adhesion). During localized tissue infection, pathogen-derived chemokines become enriched within the endothelial glycocalyx, establishing a chemotactic gradient that directs neutrophil recruitment. Intriguingly, neutrophil-derived proteolytic enzymes and reactive oxygen species released during degranulation reciprocally degrade the glycocalyx architecture, thereby amplifying chemokine liberation and creating a self-reinforcing feedback loop that potentiates neutrophil extravasation and directional migration. This review systematically analyzes two distinct mechanistic models elucidating the dual role of the endothelial glycocalyx in neutrophil chemotaxis. These conceptual frameworks advance our understanding of the spatiotemporal regulation of innate immune responses at the vascular interface while highlighting potential therapeutic targets for inflammatory disorders associated with glycocalyx dysfunction.