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Eosinophil-adhesion-inducing activity produced by antigen-stimulated mononuclear cells involves GM-CSF
1Pulmonary Division, Second Department of Internal Medicine, Saitama Medical School, Saitama, Japan. favre4mn@saitama-med.ac.jp
International Archives of Allergy and Immunology
|June 27, 2000
Summary
Granulocyte-macrophage colony-stimulating factor (GM-CSF) drives eosinophil adhesion and migration in allergic asthma. RANTES also contributes to eosinophil migration, highlighting key molecules in allergic inflammation.
Area of Science:
- Immunology
- Allergic Inflammation Research
- Respiratory Medicine
Background:
- Eosinophil accumulation in allergic inflammation begins with their adhesion to endothelial cells (EC).
- Antigen exposure upregulates eosinophil adhesive properties, likely mediated by cytokines from stimulated mononuclear cells.
Purpose of the Study:
- To identify factors from antigen-stimulated mononuclear cells that induce eosinophil adhesion and migration in atopic asthmatics.
- To investigate the role of specific cytokines and chemokines in these processes.
Main Methods:
- Peripheral blood mononuclear cells (PBMC) from asthmatics were cultured with Dermatophagoides farinae (Df) antigen.
- Eosinophil adhesion to human pulmonary microvascular endothelial cells (HPMEC) and eosinophil migration were assessed using culture supernatants.
- The effects of anti-cytokine/chemokine antibodies (anti-GM-CSF, anti-IL-5, anti-RANTES) were evaluated.
Main Results:
- Supernatants from Df-stimulated PBMC significantly increased eosinophil adhesion to HPMEC.
- This adhesion was significantly inhibited by anti-GM-CSF but not by anti-IL-5 or anti-RANTES.
- Eosinophil migration was inhibited by anti-GM-CSF and partly by anti-RANTES.
Conclusions:
- Granulocyte-macrophage colony-stimulating factor (GM-CSF) is involved in both eosinophil adhesion and migration induced by antigen-stimulated PBMC.
- RANTES plays a role specifically in eosinophil migration.
- GM-CSF and RANTES are implicated in eosinophil accumulation at allergic inflammation sites.