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Updated: Jan 7, 2026

A Microphysiological System to Study Leukocyte-Endothelial Cell Interaction during Inflammation
Published on: December 9, 2021
The eNAMPT-Integrin α5β1 Axis Mediates Neutrophil-Endothelial Cell Interactions Driving Inflammation in Ulcerative
Yongcheng Di1,2, Wenbin Ji1,2, Wenhao Xiong1,2
1Department of General Surgery, Tianjin Medical University General Hospital, Tianjin, People's Republic of China.
Background:
Ulcerative colitis (UC), a chronic inflammatory bowel disease with rising global incidence, involves neutrophil-driven mucosal damage. The precise mechanisms remain elusive, hindering targeted therapies. Therefore, this study aims to integrate single-cell transcriptomics with in vivo experiments to reveal the key signaling axes driving pathogenic neutrophil activation in UC.
Methods:
Single-cell transcriptomics characterized UC inflammatory microenvironments, focusing on neutrophil functional states and intercellular interactions. Based on key findings from bioinformatics analysis, we hypothesize that the eNAMPT-integrin α5β1 signaling axis drives abnormal neutrophil-endothelial cell communication and functionally validate this hypothesis in in vivo models.
Results:
Neutrophils exhibited aberrant activation and significant NAMPT overexpression in UC. Extracellular eNAMPT functioned as a signaling molecule binding endothelial integrin α5β1, mediating pathological neutrophil-endothelial crosstalk. Pharmacological blockade of the eNAMPT/integrin α5β1 axis inhibited neutrophil mucosal infiltration, reducing inflammation and tissue damage in UC mouse models.
Conclusion:
The eNAMPT-integrin α5β1-mediated neutrophil-endothelial communication axis represents a novel pathogenic pathway in UC, providing a foundation for precision therapies targeting this mechanism.
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