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*
GSF-National Research Center for Environment and Health, Institute of Experimental Hematology, München, Germany;
Institute of Immunology, Johannes Gutenberg University Mainz, Mainz, Germany; and
Division of Clinical Pharmacology, Medizinische Klinik, Klinikum Innenstadt of the Ludwig-Maximilians-University Munich, München, Germany
Mast cells can play detrimental roles in the pathophysiology and
mortality observed in anaphylaxis and other Th2-dominated allergic
diseases. In contrast, these cells contribute to protective host
defense mechanisms against parasitic worm infections. After IgE/Ag
activation, mast cells can produce multiple cytokines that may enhance
allergic inflammations, while a similar panel of Th2-related cytokines
may support immunological strategies against parasites. Here we report
that in primary mouse bone marrow-derived mast cells activated by
ionomycin or IgE/Ag, the proinflammatory mediator IL-1 (
or ß)
up-regulated production of IL-3, IL-5, IL-6, and IL-9 as well as TNF,
i.e., cytokines implicated in many inflammatory processes including
those associated with allergies and helminthic infections. IL-1 did not
induce significant cytokine release in the absence of ionomycin or
IgE/Ag, suggesting that Ca-dependent signaling was required.
IL-1-mediated enhancement of cytokine expression was confirmed at the
mRNA level by Northern blot and/or RT-PCR analysis. Our study reveals a
role for IL-1 in the up-regulation of multiple mast cell-derived
cytokines. Moreover, we identify mast cells as a novel source of IL-9.
These results are of particular importance in the light of recent
reports that strongly support a central role of IL-9 in allergic lung
inflammation and in host defense against worm
infections.
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