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*
Departments of Pathology and Microbiology and Immunology, Dalhousie University, Halifax, Nova Scotia, Canada; and
Department of Pathology, McMaster University, Hamilton, Ontario, Canada
Nerve growth factor (NGF) is well recognized to have a number of
potent effects on mast cells, including increasing mast cell numbers in
vivo and inducing mast cell degranulation in vitro. More recently, NGF
has been demonstrated to induce PGD2 production by mast
cells through the induction of mast cell cyclooxygenase expression. We
have observed that NGF at doses as low as 10 ng/ml will induce IL-6
production and inhibit TNF-
release from rat peritoneal mast cells
in the presence of lysophosphatidylserine as a cofactor. NGF synergizes
with LPS treatment of peritoneal mast cells (PMC) for the induction of
IL-6. Examination of the mechanism of this phenomenon has revealed that
NGF can induce both rat PMC and mouse bone marrow-derived cultured mast
cells to produce substantial levels of PGE2. This response
is maximal at later time points 18–24 h after NGF activation. The
ability of NGF to induce PGE2 is not dependent on mast cell
degranulation. Other stimuli capable of inducing IL-6, such as LPS, do
not induce production of this prostanoid. Inhibition of cyclooxygenase
activity by PMC using either flurbiprofen or indomethacin inhibited
both the NGF-induced PGE2 synthesis and the NGF-induced
alterations in TNF- and IL-6 production. These results suggest a
role for mast cell-derived prostanoids in the regulation of local
inflammatory responses and neuronal degeneration after tissue injury
involving induction of NGF production.
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