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The Journal of Immunology, 2000, 165: 6545-6552.
Copyright © 2000 by The American Association of Immunologists

Prostaglandin E2 Selectively Enhances the IgE-Mediated Production of IL-6 and Granulocyte-Macrophage Colony-Stimulating Factor by Mast Cells Through an EP1/EP3-Dependent Mechanism1

Kaede Gomi*, Fu-Gang Zhu* and Jean S. Marshall2,*,{dagger}

Departments of * Microbiology and Immunology, and {dagger} Pathology, Dalhousie University, Halifax, Nova Scotia, Canada

PGE2 is an endogenously synthesized inflammatory mediator that is over-produced in chronic inflammatory disorders such as allergic asthma. In this study, we investigated the regulatory effects of PGE2 on mast cell degranulation and the production of cytokines relevant to allergic disease. Murine bone marrow-derived mast cells (BMMC) were treated with PGE2 alone or in the context of IgE-mediated activation. PGE2 treatment alone specifically enhanced IL-6 production, and neither induced nor inhibited degranulation and the release of other mast cell cytokines, including IL-4, IL-10, IFN-{gamma}, and GM-CSF. IgE/Ag-mediated activation of BMMC induced the secretion of IL-4, IL-6, and GM-CSF, and concurrent PGE2 stimulation synergistically increased mast cell degranulation and IL-6 and GM-CSF, but not IL-4, production. A similar potentiation of degranulation and IL-6 production by PGE2, in the context of IgE-directed activation, was observed in the well-established IL-3-dependent murine mast cell line, MC/9. RT-PCR analysis of unstimulated MC/9 cells revealed the expression of EP1, EP3, and EP4 PGE receptor subtypes, including a novel splice variant of the EP1 receptor. Pharmacological studies using PGE receptor subtype-selective analogs showed that the potentiation of IgE/Ag-induced degranulation and IL-6 production by PGE2 is mediated through EP1 and/or EP3 receptors. Our results suggest that PGE2 may profoundly alter the nature of the mast cell degranulation and cytokine responses at sites of allergic inflammation through an EP1/EP3-dependent mechanism.




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