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Analysis of Physiologic E-Selectin-Mediated Leukocyte Rolling on Microvascular Endothelium
Published on: February 11, 2009
L-selectin shear thresholding modulates leukocyte secondary capture
Christopher D Paschall1, Michael B Lawrence
1Department of Biomedical Engineering, University of Virginia, 415 Lane Road, Charlottesville, VA 22908, USA.
Annals of Biomedical Engineering
|February 27, 2008
Summary
Leukocyte secondary capture, crucial for inflammation, is regulated by L-selectin mediated shear thresholding. This process amplifies leukocyte accumulation at high shear stresses, impacting inflammatory responses.
Area of Science:
- Immunology
- Biophysics
Background:
- Leukocyte accumulation at inflammation sites involves transient homotypic adhesions.
- Primary leukocyte capture relies on P-selectin and PSGL-1; secondary capture involves PSGL-1 and L-selectin interactions.
Purpose of the Study:
- To investigate the role of L-selectin in mediating leukocyte secondary capture and string formation.
- To analyze the impact of hydrodynamic shear thresholding on leukocyte secondary capture.
Main Methods:
- Developed a novel quantitative method to analyze leukocyte string formation in vitro.
- Utilized L-selectin monoclonal antibody (mAb) DREG-56 to assess adhesion's contribution.
Main Results:
- Hydrodynamic shear thresholding inhibited secondary capture at low shear stresses but amplified it at high shear stresses.
- Addition of DREG-56 significantly inhibited leukocyte string formation.
- Data suggest L-selectin mediated shear thresholding modulates secondary capture.
Conclusions:
- L-selectin mediated shear thresholding plays a significant role in regulating leukocyte secondary capture.
- This mechanism complements previously described hydrodynamic recruitment mechanisms in inflammation.
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