Dexamethasone potently induces human basophil apoptosis
N. Suzaki, Y. Tanimoto, M. Sakugawa, N. Hamada, K. Takao, A. Kanehiro, K. Ikeda, M. Kataoka, M. Tanimoto, K. Imajo, K. Takahashi (Okayama, Hayashima, Japan)
Source: Annual Congress 2002 - Cellular reactions in allergy in humans and animals
Session: Cellular reactions in allergy in humans and animals
Session type: Poster Discussion
Number: 306
Disease area: Airway diseases
Abstract Basophils are known to be involved in late-phase allergic reactions concomitant with eosinophils and T-lymphocytes. Glucocorticoids have been widely used in the treatment of allergic diseases. Their anti-inflammatory properties may include inhibition of basophil functions such as mediator release and cytokine production. To clarify the effects of glucocorticoids on human basophil survival, we observed apoptosis of basophils cultured with glucocorticoids in the presence or absence of a basophil growth factor, interleukin (IL)-3. A large number of basophils (purity > 95%) were obtained by culturing peripheral blood stem cell-rich mononuclear cells with IL-3 followed by negative selection using immunomagnetic beads. These basophils were then incubated with dexamethasone (DEX) and/or IL-3. The degree of basophil apoptosis was assessed by double-stain using annexin V and propidium iodide. DEX (10-6 -10-9 M) induced basophil apoptosis in a dose-dependent manner. On the other hand, IL-3 (5pg/ml-5ng/ml) had a potent antiapoptotic effect. This effect at low concentrations of IL-3 (5-50pg/ml) was partially inhibited by DEX, although relatively high concentrations of IL-3 (0.5-5ng/ml) could overcome the apoptotic effect of DEX. These findings indicate the therapeutic efficacy of glucocorticoids in chronic allergic diseases such as bronchial asthma might result from promoting basophil apoptosis at least in part.
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N. Suzaki, Y. Tanimoto, M. Sakugawa, N. Hamada, K. Takao, A. Kanehiro, K. Ikeda, M. Kataoka, M. Tanimoto, K. Imajo, K. Takahashi (Okayama, Hayashima, Japan). Dexamethasone potently induces human basophil apoptosis. Eur Respir J 2002; 20: Suppl. 38, 306
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