Abstract
The mode of action of corticosteroids, important drugs in the treatment of inflammatory disease, is not yet fully understood. Corticosteroids are known to inhibit phospholipase A2 in unprimed eosinophils and basophils, preventing leukotriene synthesis, but their effect on cells that are already primed is unknown. As inflammatory cells from atopic subjects are often primed in vivo, we studied the effects of two potent corticosteroids on basophil sulfidoleukotriene production in peripheral blood mixed leukocytes (PBML) from in-season and out-of-season atopic individuals. Cells were incubated for 24 hours with mometasone furoate or beclomethasone dipropionate, primed with IL-3, stimulated with calcium ionophore, buffer, allergen or anti-IgE, and leukotriene production was quantified. Peripheral blood mononuclear leukocytes from five of ten donors (in season) produced elevated sulfidoleukotrienes without a stimulus; cells from seven donors responded to anti-IgE by increased sulfidoleukotrienes. Neither steroid consistently affected sulfidoleukotriene production in anti-IgE-stimulated cells which were releasing sulfidoleukotrienes in the absence of a stimulant. In comparison, sulfidoleukotriene production was significantly reduced b...Continue Reading
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