Related Experiment Video
Updated: Aug 11, 2026

Tracking Neutrophil Intraluminal Crawling, Transendothelial Migration and Chemotaxis in Tissue by Intravital Video Microscopy
Published on: September 24, 2011
Neutrophil Mac-1 and MEL-14 adhesion proteins inversely regulated by chemotactic factors
T K Kishimoto1, M A Jutila, E L Berg
1Department of Pathology, Stanford University, CA 94305.
Abstract:
The neutrophil Mac-1 and gp100MEL-14 adhesion proteins are involved in neutrophil extravasation during inflammation. Both the expression and activity of Mac-1 are greatly increased after neutrophil activation. In contrast, neutrophils shed gp100MEL-14 from the cell surface within 4 minutes after activation with chemotactic factors or phorbol esters, releasing a 96-kilodalton fragment of the antigen into the supernatant. Immunohistology showed that gp100MEL-14 was downregulated on neutrophils that had extravasated into inflamed tissue. The gp100MEL-14 adhesion protein may participate in the binding of unactivated neutrophils to the endothelium; rapid shedding of gp100MEL-14 may prevent extravasation into and damage of normal tissues by activated neutrophils.
Insights
Neutrophil Mac-1 increases with activation, while gp100MEL-14 sheds rapidly. This shedding may prevent activated neutrophils from damaging healthy tissues during inflammation.
Area of Science:
- Immunology
- Cell Biology
- Inflammation Research
Background:
- Neutrophil extravasation is crucial during inflammation, involving adhesion proteins like Mac-1 and gp100MEL-14.
- Mac-1 expression and activity significantly increase upon neutrophil activation.
- gp100MEL-14 is rapidly shed from the neutrophil surface after activation.
Purpose of the Study:
- To investigate the role of gp100MEL-14 shedding in neutrophil function during inflammation.
- To understand the differential regulation of Mac-1 and gp100MEL-14 during neutrophil activation and extravasation.
Main Methods:
- Neutrophil activation assays using chemotactic factors and phorbol esters.
- Measurement of Mac-1 and gp100MEL-14 expression and shedding.
- Immunohistochemical analysis of gp100MEL-14 on extravasated neutrophils in inflamed tissue.
Main Results:
- Neutrophil activation led to a rapid shedding of gp100MEL-14, releasing a 96-kDa fragment.
- gp100MEL-14 was downregulated on neutrophils that had extravasated into inflamed tissue.
- Mac-1 expression and activity were upregulated following neutrophil activation.
Conclusions:
- Rapid shedding of gp100MEL-14 upon activation is a key regulatory mechanism.
- This shedding may prevent activated neutrophils from binding to and damaging healthy endothelium.
- gp100MEL-14 might play a role in the initial adhesion of unactivated neutrophils to the endothelium.
Related Concept Videos
Cell Polarization by Rho Proteins
Chemotaxis and Direction of Cell Migration
Intracellular Signaling Affects Focal Adhesions
Some...
Selectins
Immunoglobulin-like Cell Adhesion Molecules
Ig-CAMs exhibit either homophilic binding (to other Ig-CAMs) or heterophilic binding (to other ligands such as integrins). While most Ig-CAMs...
Chemotaxis in E. coli

