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B1
Department of Psychiatry, University of Freiburg Medical School, Freiburg, Germany
Substance P (SP), a member of the tachykinin peptide family, is a
major mediator of neuroimmunomodulatory activities and neurogenic
inflammation within the central and peripheral nervous system. SP has
been shown to induce the expression of proinflammatory cytokines such
as IL-6, which might be implicated in the etiopathology of several
human brain disorders. We showed in a previous study that nanomolar
concentrations of SP triggered activation of NF-
B, a transcription
factor involved in the control of cytokine expression. However,
activation of NF-B was not involved in SP-induced expression of
IL-6. Here, we describe p38 mitogen-activated protein kinase (p38 MAPK)
as a signal transduction component that operates independently from
NF-B activation and that mediates SP-induced IL-6 expression in the
human astrocytoma cell line U373 MG. SP induced the phosphorylation of
p38 MAPK within 10 min, and this activation persisted up to 30 min and
was independent from p42/44 MAPKs and protein kinase C activation,
which all are induced after stimulation with SP. As shown by EMSA, p38
MAPK was not involved in SP-induced activation of NF-B. p38 MAPK,
however, mediated SP-induced IL-6 expression as shown by the use of
specific inhibitors of this kinase. Our results suggest that activation
of p38 MAPK is an important component controlling neurogenic
inflammation within the CNS independently from NF-B. Drugs targeting
this MAPK may therefore interfere with SP-correlated neuropsychiatric
disorders and may represent a therapeutic approach in these
disorders.
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