Glucocorticoids induce basophil apoptosis

Background: Induction of apoptosis represents an important mechanism by whi ch glucocorticoids (GCCs) exert their antiinflammatory properties. The effe cts of GCCs on apoptosis have been determined in various immune cells and f ound to vary among different cell types. On the other hand, the effects of GCCs on apoptosis of basophils, active participants in allergic inflammatio n, have remained obscure. Objective: The objective of this study was to investigate the effects of GC Cs on basophil apoptosis. Methods: Basophils were highly purified (purity, >97%) by Percoll density g radient centrifugation followed by negative selection. Cell status was dete rmined by their ability to bind annexin V and exclude propidium iodide. DNA fragmentation was determined by Dow cytometry. Results: Dexamethasone (DEX) significantly accelerated the decrease in live cells and increased the number of apoptotic cells in a time-dependent fash ion. Light microscopy as well as DNA fragmentation assay confirmed the indu ction of apoptosis by DEX. A half-maximal effect was observed in a DEX conc entration range from 10(-9) to 10(-8) mol/L. Sex steroids did not induce ba sophil apoptosis at all. DEX also induced basophil apoptosis in the presenc e of low doses of IL-3. Conclusion: GCCs exert potent apoptogenic effects on basophils. GCC-mediate d apoptogenic effects on basophils might have implications with respect to the mechanism of action of this class of drugs in allergic disorders.