IL-3 Primes and Evokes Histamine Release from Human Basophils but not Mast Cells

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Abstract
To assess the effect of IL-3 on mediator release from human histamine-containing cells, we have investigated IL-3 induced histamine release (HR) and IL-3 priming of IgE-dependent and IgE-independent HR from human basophils and mast cells dispersed from human skin, tonsil and lung. Mixed leukocytes from selected atopic subjects, whose basophils release histamine in response to IL-3, were prepared by dextran sedimentation. Mast cells were enzymatically dispersed using collagenase and hyaluronidase. IL-3, 0.1–100 ng/ml, caused a concentration-dependent HR from basophils which required both extracellular Ca2+ and the presence of membrane IgE. No release was seen from mast cells. Desensitization of basophils to anti-IgE by lactate stripping or challenge in a Ca2+-free medium blocked IL-3-induced HR. IL-3 primed basophils, but not mast cells, for HR induced fMLP by a mechanism which was independent of the presence of both cell surface IgE and extracellular Ca2+. This priming effect was not blocked by desensitization of cells to anti-IgE. IL-3 priming of IgE- and fMLP-induced HR occurred in the same concentration range as did IL-3-evoked HR. When two secretagogues, IL-3 and anti-IgE or fMLP, were combined, the result was additive or supra-additive depending on the basophil donor. The protein kinase C (PKC) inhibitor staurosporine, 10 nM, inhibited anti-IgE-induced HR but neither IL-3-induced HR nor priming. Pertussis toxin (PT), 1.0 μg/ml, inhibited fMLP-induced HR although anti-IgE-induced HR, IL-3-evoked HR and IL-3 priming of anti-IgE-induced HR were unaltered. These results indicate that IL-3 modulates HR from human basophils by two mechanisms: a direct release which involves the mechanisms induced by cell surface IgE, but which is unlikely to proceed by the same mechanism as cross-linkage of IgE by anti-IgE, and a priming effect which is independent of IgE and extracellular Ca2+.

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