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Related Experiment Videos

Endothelial cells upregulate eosinophil superoxide generation via VCAM-1 expression.

M Nagata1, J B Sedgwick, R Vrtis

  • 1Pulmonary Division, Second Department of Internal Medicine, Saitama Medical School, Saitama, Japan.

Clinical and Experimental Allergy : Journal of the British Society for Allergy and Clinical Immunology
|April 15, 1999
PubMed
Summary

Eosinophil (EOS) adhesion to endothelial cells via VLA-4/VCAM-1 interaction enhances inflammatory function. This process, along with platelet-activating factor (PAF), primes EOS for increased superoxide anion generation during airway inflammation.

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Area of Science:

  • Immunology
  • Cell Biology
  • Respiratory Medicine

Background:

  • Eosinophil (EOS) adhesion to vascular cell adhesion molecule-1 (VCAM-1) stimulates superoxide anion (O2-) generation.
  • EOS adhesion via VLA-4 to VCAM-1 on endothelium may be crucial for EOS recruitment and function in airway inflammation.

Purpose of the Study:

  • To investigate if EOS interaction with endothelial cells expressing VCAM-1 enhances inflammatory function.
  • To determine the mechanisms underlying EOS activation in the context of endothelial cell interaction.

Main Methods:

  • Human umbilical vein endothelial cells (HUVEC) were stimulated with interleukin (IL)-4 and tumor necrosis factor (TNF)-alpha.
  • EOS adhesion and O2- generation were measured using enzyme-linked immunosorbent assay and flow cytometry.

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  • Monoclonal antibodies and platelet-activating factor (PAF) antagonist were used to block specific interactions and pathways.

    • Main Results:

    • IL-4 and TNF-alpha synergistically induced VCAM-1 expression on HUVEC, increasing EOS adhesion and priming O2- generation.
    • EOS adhesion was partially inhibited by anti-VLA-4 and anti-beta2 antibodies, while O2- generation was fully inhibited by anti-VLA-4 or anti-VCAM-1 antibodies.
    • Enhanced O2- generation, but not adhesion, was inhibited by a PAF antagonist, suggesting PAF's role in priming EOS.

    Conclusions:

    • EOS adhesion to endothelial cells via VLA-4/VCAM-1 interaction is important for EOS function development.
    • EOS function modulation involves both adhesion to VCAM-1-expressing HUVEC and platelet-activating factor (PAF).