Human endothelial cells prolong eosinophil survival. Regulation by cytokines and glucocorticoids.
Many recent studies have established the eosinophil as an active proinflammatory participant in a variety of disease states, most notably in allergic and helminthic disorders. In order to understand the effector role of eosinophils, factors which promote a selective eosinophilic infiltrate must be delineated. Eosinophil adherence to vascular endothelium is the first step in the formation of such an infiltrate. However, studies thus far have failed to identify factors which selectively activate the adherence of eosinophils. We have therefore speculated that the selective enrichment of eosinophils may result from nonselective recruitment of several leukocyte types combined with the production of local factors that promote the survival of eosinophils and not of other cells. We report that endothelial cell-conditioned medium selectively prolongs eosinophil survival up to 6 days in culture in a dose- and time-dependent manner. Stimulation of human vascular endothelial cells with IL-1 caused an increase in the generation of eosinophil survival-promoting activity, whereas stimulation with platelet-activating factor did not. Supernatants from human vascular endothelial cells cultured for 48 h in the presence of the glucocorticoid, dexamethasone, were less active in promoting eosinophil survival than control supernatants. These results suggest that factors produced locally in the vascular microenvironment may selectively promote eosinophil survival and may be under the regulation of cytokines and glucocorticoids.
Lamas
A M
AM
Johns Hopkins University School of Medicine, Good Samaritan Hospital, Baltimore, MD 21239.
Marcotte
G V
GV
Schleimer
R P
RP
D001685:Biological Factors / Q000494:pharmacology*; D002469:Cell Separation; D002470:Cell Survival / Q000187:drug effects; D002474:Cell-Free System; D002478:Cells, Cultured; D016207:Cytokines; D003907:Dexamethasone / Q000494:pharmacology*; D004730:Endothelium, Vascular / Q000032:analysis / Q000502:physiology*; D004804:Eosinophils / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D006801:Humans; D007375:Interleukin-1 / Q000494:pharmacology; D007958:Leukocyte Count
D001685:Biological Factors; D016207:Cytokines; D007375:Interleukin-1; D003907:Dexamethasone