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KMID : 0377619960610120961
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Korean Jungang Medical Journal
1996 Volume.61 No. 12 p.961 ~ p.961
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The Interaction of Cytokine and Glucocorticoid in the Programmed Cell Death of Eosinophils
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Erk Her
K. Frank Austen
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Abstract
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The in vitro viability and the physical and functional phenotype of human peripheral blood eosinophils are regulated by the action of granulocyte-macrophage colony-stimulating factor(GM -CSF), interleukin-3(IL-3), and IL-5. In the idiopathic hypereosinophils syndrome and the tryptophan-associated eosinophilia/myalgia syndrome, the presence of hypodence eosinophils in the blood is associated with excessive serum levels of IL-5. The aim of study was to characterize, and to utilize this model cell system to determine the endothelial cell-mediated interactions of IL-1 and dexamethasone on eosinophil viability. GMCSF was established as the constitutive and elicited human umbilical vein endothelial cell-derived eosinophil viability-sustaining factor. Stimulation of endothelium cell monolayers with interleukin-1 (IL-1 ; 5 U/ml) increased the 48-h elaboration of GM-CSF from a mean of 3.2 to a mean of 8.2 pM(p <0.05). Dexamethasone(100 nM) decreased the constitutive GM-CSF elaboration by 49%(p<0.001) but did not diminish production by IL-1-stimulated endothelium. However, eosinophil viability decreased by 21% in dexamethasone-pretreated IL-l-stimulated endothelial cell-conditioned medium(p <0.05), which suggested viability antagonism by glucocorticoids. After 24h of culture, eosinoph1 l viability for replicate cells in enriched medium alone or with l pm GM -CSF decreased from means of 43 and 75 % to means of 21 and 54%, respectively, when dexamethasone was induced(p <0.05). However, 10 pM GM-CSF, IL-3, or IL-5 protected the cells against dexamethasone and against endonucleasesspecific DNA fragmentation. In this model system of eosinophil-tissue interactions, dexamethasone prevents the endothelial cells from inducing a pathologic phenotypic change in the eosinophil by suppression of GM-CSF elaboration to concentration that are not cytoprotective. Cytokine priming by GM-CSF, IL-3, or IL-5 may account for the differential responsiveness of eosinophillic disorders to glucocorticoids.
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KEYWORD
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