Activation of HUVEC monolayers by IL-1β or TNF-α induces migration of eosinophils across the endothelial monolayer (i.e., transendothelial migration) in vitro. In the present study, we demonstrate that culture of freshly isolated eosinophils in the presence of IL-5 for 24 to 48-h before use in the assay dramatically potentiated CD18-dependent eosinophil transendothelial migration through unstimulated endothelial monolayers. Granulocyte macrophage (GM)-CSF induced eosinophil transendothelial migration but did not induce neutrophil transendothelial migration. When IL-1β- activated endothelial cells were used, GM-CSF, IL-3, or IL-5 caused only modest potentiation of eosinophil transendothelial migration. Since activated endothelial cells are known to produce GM-CSF, we hypothesized that endothelial-derived GM-CSF might play a role in the process of IL-1β- induced eosinophil transendothelial migration. IL-1β-activated endothelial monolayers grown on the permeable supports produced 0.3 ± 0.1 ng/ml of GM- CSF during a 4-h incubation and neutralizing Ab against GM-CSF inhibited eosinophil transendothelial migration by 48%, suggesting that endothelial- derived GM-CSF may participate in the response. Eosinophils purified from bronchoalveolar lavage 18 to 20 h after experimental Ag challenge in the lungs of allergic volunteers showed enhanced transendothelial migration, indicating that the cells may have undergone cytokine activation in vivo. Eosinophil-active cytokines may contribute to the preferential accumulation of eosinophils in vivo in part via potentiation of eosinophil transendothelial migration.
|Original language||English (US)|
|Number of pages||7|
|Journal||Journal of Immunology|
|State||Published - May 1 1994|
ASJC Scopus subject areas
- Immunology and Allergy