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Endothelial adhesion molecules and their role in inflammation
1Department of Pediatrics, Baylor College of Medicine, Houston, TX.
Canadian Journal of Physiology and Pharmacology
|January 1, 1993
Summary
Neutrophil rolling and adhesion to blood vessel walls involve selectins and integrins. Blocking these molecules, like CD18 and ICAM-1, significantly reduces neutrophil migration to inflammatory sites.
Area of Science:
- Immunology
- Cell Biology
- Vascular Biology
Background:
- Leukocyte emigration into inflammatory sites is crucial for immune response.
- Neutrophil margination and rolling are initial steps mediated by selectin adhesion molecules.
- Selectins (E-selectin, P-selectin, L-selectin) facilitate neutrophil rolling via carbohydrate recognition.
Purpose of the Study:
- To elucidate the molecular mechanisms of neutrophil adhesion and transmigration.
- To investigate the roles of selectins and integrins in leukocyte emigration.
Main Methods:
- In vitro studies using endothelial cell cultures.
- In vivo animal models of inflammation.
- Utilized monoclonal antibodies to block specific adhesion molecules.
Main Results:
- Selectins mediate initial neutrophil rolling on endothelium.
- Chemotactic factors trigger a switch from selectin-dependent to beta 2-integrin (CD11a/CD18, CD11b/CD18) mediated adhesion.
- Blocking CD18 integrins or ICAM-1 significantly inhibits transendothelial migration in vitro.
- Antibodies against selectins, CD18, CD11a, CD11b, and ICAM-1 reduce neutrophil influx in animal models.
Conclusions:
- Neutrophil adhesion and emigration are complex, multi-step processes involving selectins and integrins.
- Targeting these adhesion molecules offers potential therapeutic strategies for inflammatory diseases.