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Updated: Aug 15, 2026

Quantitative In vitro Assay to Measure Neutrophil Adhesion to Activated Primary Human Microvascular Endothelial Cells under Static Conditions
11:22

Quantitative In vitro Assay to Measure Neutrophil Adhesion to Activated Primary Human Microvascular Endothelial Cells under Static Conditions

Published on: August 23, 2013

Transient adhesion of neutrophils to endothelium

S K Lo1, P A Detmers, S M Levin

  • 1Laboratory of Cellular Physiology and Immunology, Rockefeller University, New York, New York 10021.

The Journal of Experimental Medicine
|May 1, 1989
PubMed

Insights

Transient adhesion of polymorphonuclear leukocytes (PMN) to endothelial cells (EC) depends on CD11/CD18 molecules. Adhesion is regulated by changes in existing CD11/CD18, not necessarily increased expression, highlighting a dynamic regulatory mechanism.

Area of Science:

  • Immunology
  • Cell Biology
  • Biochemistry

Background:

  • Polymorphonuclear leukocytes (PMN) play a crucial role in inflammatory responses.
  • Endothelial cells (EC) are key participants in regulating leukocyte trafficking.
  • The interaction between PMN and EC is critical for immune cell migration to sites of inflammation.

Purpose of the Study:

  • To investigate the mechanisms regulating the transient adhesion of PMN to EC.
  • To determine the role of CD11/CD18 integrins in PMN-EC adhesion.
  • To elucidate whether changes in CD11/CD18 expression or function mediate adhesion dynamics.

Main Methods:

  • Utilized fluorescently labeled PMN and in vitro cultured human umbilical vein EC.
  • Stimulated PMN with phorbol dibutyrate (PDB), TNF, and C5a to induce adhesion.
  • Employed CD11/CD18-deficient PMN, anti-CD18 monoclonal antibodies (mAbs), and cytoplasts to assess molecular contributions.

Main Results:

  • PMN adhesion to EC increased upon stimulation but returned to baseline levels over time.
  • Adhesion was completely dependent on CD11/CD18 integrins, with both CD11a/CD18 and CD11b/CD18 contributing.
  • Transient adhesion occurred even in cytoplasts lacking increased CD11b/CD18 expression, suggesting functional modulation.

Conclusions:

  • The transient adhesion of stimulated PMN to EC is primarily regulated by alterations in the functional state of existing CD11/CD18 molecules.
  • While increased CD11b/CD18 expression may contribute, it is not the sole determinant of enhanced PMN adhesivity.
  • This study highlights a dynamic regulation of integrin function in controlling leukocyte adhesion during inflammation.

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