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Adhesion mechanisms involved in C5a-induced eosinophil homotypic aggregation
M M Teixeira1, A G Rossi, P G Hellewell
1Applied Pharmacology, National Heart and Lung Institute, Imperial College of Science, Technology and Medicine, London, England.
Journal of Leukocyte Biology
|March 1, 1996
Summary
Guinea pig eosinophil aggregation relies mainly on CD11/CD18 and L-selectin adhesion molecules. Very late antigen-4 (VLA-4) does not play a role in this homotypic aggregation process.
Area of Science:
- Immunology
- Cell Biology
- Biochemistry
Background:
- Leukocytes interact with endothelial cells and each other during tissue migration.
- Understanding eosinophil homotypic aggregation mechanisms is crucial for inflammatory response research.
Purpose of the Study:
- To investigate the adhesion molecules involved in guinea pig eosinophil homotypic aggregation.
- To elucidate the roles of CD11/CD18, ICAM-1, VLA-4, and L-selectin in eosinophil aggregation.
Main Methods:
- Assessed eosinophil aggregation using light transmission changes.
- Utilized monoclonal antibodies (mAbs) against CD18, ICAM-1, and VLA-4.
- Investigated L-selectin involvement using heparin, fucoidin, and anti-L-selectin mAb MEL-14.
Main Results:
- Anti-CD18 mAb partially inhibited C5a-induced eosinophil aggregation.
- Anti-ICAM-1 and anti-VLA-4 mAbs had no significant effect on aggregation.
- Heparin, fucoidin, and anti-L-selectin mAb MEL-14 effectively inhibited eosinophil aggregation.
Conclusions:
- Guinea pig eosinophil homotypic aggregation is primarily mediated by CD11/CD18 and L-selectin.
- VLA-4 does not play a role in guinea pig eosinophil aggregation.