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,
*
Department of Medicine, Harvard Medical School, Boston, MA 02115;
Division of Rheumatology, Immunology, and Allergy, and
Partners’ Asthma Center, Brigham and Women’s Hospital, Boston, MA 02115; and
Osaka Bioscience Institute, Osaka, Japan
Mouse bone marrow-derived mast cells (BMMC), stimulated with stem
cell factor, IL-1
, and IL-10, secrete IL-6 and demonstrate a delayed
phase of PGD2 generation that is dependent upon the induced
expression of PG endoperoxide synthase (PGHS)-2. We have examined the
potential for exogenous prostanoids, acting in a paracrine fashion, and
endogenous prostanoids, acting in an autocrine fashion, to regulate
PGHS-2 induction and IL-6 secretion in mouse BMMC. Exogenous
PGE2, which acts through G protein-coupled receptors, and
15-deoxy-
12,14-PGJ2, which is a ligand for
peroxisome proliferator-activated receptor (PPAR)
, elicited a 2- to
3-fold amplification of PGHS-2 induction, delayed-phase
PGD2 generation, and IL-6 secretion in response to stem
cell factor, IL-1, and IL-10. The effect of PGE2 was
reproduced by the E prostanoid (EP)1 receptor agonist
17-trinor-PGE2, and the EP1/EP3 agonist, sulprostone, but
not the EP2 receptor agonist, butaprost. Although BMMC express PPAR,
the effects of 15-deoxy-12,14-PGJ2 were not
reproduced by the PPAR agonists, troglitazone and ciglitazone.
PGHS-2 induction, but not IL-6 secretion, was impaired in
cPLA2-deficient BMMC. However, there was no impairment of
PGHS-2 induction in BMMC deficient in hematopoietic PGD synthase or
PGHS-1 in the presence or absence of the PGHS-2 inhibitor, NS-398.
Thus, although exogenous prostanoids may contribute to amplification of
the inflammatory response by augmenting PGD2 generation and
IL-6 secretion from mast cells, endogenous prostanoids do not play a
role.
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