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已发表论文
中性粒细胞趋化作用中血管内皮糖萼参与模型
Authors Li P, Si Z, Shao Y, Wu W
Received 26 June 2025
Accepted for publication 4 November 2025
Published 17 November 2025 Volume 2025:18 Pages 7025—7036
DOI https://doi.org/10.2147/IJGM.S549797
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Gauri Agarwal
Ping Li,1,* Zhengwang Si,2,* Yiming Shao,2 Weiwei Wu1
1Department of Burns Surgery, The First Hospital of Jilin University, Changchun, Jilin, 130000, People’s Republic of China; 2Department of Burns Surgery, Affiliated Hospital of Jining Medical University, Jining Medical University, Jining, Shandong, 272000, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Weiwei Wu, Department of Burns Surgery, The First Hospital of Jilin University, Changchun, Jilin, 130000, People’s Republic of China, Email jdsswk_www@163.com Yiming Shao, Department of Burns Surgery, Affiliated Hospital of Jining Medical University, Jining Medical University, Jining, Shandong, 272000, People’s Republic of China, Email symlcyb@163.com
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.
Keywords: neutrophil, chemokines, endothelial glycocalyx
1Department of Burns Surgery, The First Hospital of Jilin University, Changchun, Jilin, 130000, People’s Republic of China; 2Department of Burns Surgery, Affiliated Hospital of Jining Medical University, Jining Medical University, Jining, Shandong, 272000, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Weiwei Wu, Department of Burns Surgery, The First Hospital of Jilin University, Changchun, Jilin, 130000, People’s Republic of China, Email jdsswk_www@163.com Yiming Shao, Department of Burns Surgery, Affiliated Hospital of Jining Medical University, Jining Medical University, Jining, Shandong, 272000, People’s Republic of China, Email symlcyb@163.com
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.
Keywords: neutrophil, chemokines, endothelial glycocalyx