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Related Experiment Videos

Adhesion molecules and inflammatory injury

S M Albelda1, C W Smith, P A Ward

  • 1Department of Medicine, University of Pennsylvania Medical Center, Philadelphia 19104.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|May 1, 1994
PubMed
Summary

Cell adhesion molecules (CAMs) mediate neutrophil-endothelial cell interactions during inflammation. Targeting specific CAMs offers a promising strategy for treating various inflammatory diseases.

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Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Medicine

Background:

  • Neutrophil-endothelial cell interactions are crucial for inflammation, involving a cascade of adhesion molecules and chemoattractants.
  • Selectins mediate initial neutrophil slowing, while integrins like CD11/CD18 bind to endothelial ligands (e.g., ICAM-1) for firm adhesion.
  • Transmigration requires chemotactic stimuli and platelet-endothelial cell adhesion molecule-1 (PECAM-1) engagement.

Purpose of the Study:

  • To investigate the role of cell adhesion molecules (CAMs) in vivo during inflammatory processes.
  • To explore the potential of targeting CAMs for therapeutic interventions in inflammatory diseases.

Main Methods:

  • Utilized blocking antibodies against CAMs.
  • Employed chimeric selectin-immunoglobulin proteins.

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  • Studied sialyl Lewisx oligosaccharides and peptides.
  • Examined humans and animals with genetic adhesion deficiencies.

    • Main Results:

    • CAM blockade effectively inhibits inflammation in vivo.
    • Distinct adhesion requirements exist for different types of inflammation.
    • Understanding CAM/chemoattractant profiles is key to targeted therapy.

    Conclusions:

    • Cell adhesion molecules play a critical role in the inflammatory response.
    • Targeting specific CAMs and chemoattractant pathways holds potential for precise and effective treatment of inflammatory diseases.