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B Is Decisively Involved in the Expression of IL-91
*
Institute of Immunology, Johannes Gutenberg University, Mainz, Germany;
Gesellschaft für Strahlen und Umweltforschung-National Research Center for Environment and Health, Institute of Clinical Molecular Biology and Tumor Genetics, Munich, Germany; and
Institute of Pathology, University of Wurzburg, Wurzburg, Germany
Mast cells, due to their ability to produce a large panel of
mediators and cytokines, participate in a variety of processes in
adaptive and innate immunity. Herein we report that in primary murine
bone marrow-derived mast cells activated with ionomycin or IgE-Ag the
bacterial endotoxin LPS strongly enhances the expression of IL-9 and
IL-13, but not IL-4. This costimulatory effect of LPS is absent in
activated mast cells derived from the LPS-hyporesponsive mouse strain
BALB/c-LPSd, although in these cells the
proinflammatory cytokine IL-1 can still substitute for LPS. The
enhanced production of mast cell-derived IL-13 in the presence of IL-1
is a novel observation. Coactivation of mast cells with LPS leads to a
synergistic activation of NF-
B, which is shown by an NF-B-driven
reporter gene construct. In the presence of an inhibitor of NF-B
activation, the production of IL-9 is strongly decreased, whereas the
expression of IL-13 is hardly reduced, and that of IL-4 is not affected
at all. NF-B drives the expression of IL-9 via three NF-B binding
sites within the IL-9 promoter, which we characterize using gel shift
analyses and reporter gene assays. In the light of recent reports that
strongly support critical roles for IL-9 and IL-13 in allergic lung
inflammation, our results emphasize the potential clinical importance
of LPS as an enhancer of mast cell-derived IL-9 and IL-13 production in
the course of inflammatory reactions and allergic
diseases.
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