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-Induced Janus Kinase-1-STAT1 Activation in Macrophages by Vasoactive Intestinal Peptide and Pituitary Adenylate Cyclase-Activating Polypeptide
*
Department of Biological Sciences, Rutgers University, Newark, NJ 07102; and
Departamento Biologia Celular, Facultad de Biologia, Universidad Complutense, Madrid, Spain
The vasoactive intestinal peptide (VIP) and the pituitary adenylate
cyclase-activating polypeptide (PACAP), two immunomodulatory
neuropeptides that affect both innate and acquired immunity,
down-regulate IL-12 p40 and inducible NO synthase expression in
LPS/IFN-
-stimulated macrophages. We showed previously that VIP/PACAP
inhibit NF-
B nuclear translocation through the stabilization of
IB and reduce IFN regulatory factor-1 (IRF-1) binding to the
regulatory elements found in the IL-12 p40 and inducible NO synthase
promoters. In this paper we studied the molecular mechanisms involved
in the VIP/PACAP regulation of IRF-1 transactivating activity. Our
studies indicate that the inhibition in IRF-1 binding correlates with a
reduction in IRF-1 protein and mRNA in IFN--treated Raw 264.7
macrophages. In agreement with the described Janus kinase
(Jak)1/Jak2/STAT1/IRF-1 activation pathway, VIP/PACAP inhibit
Jak1/Jak2, STAT1 phosphorylation, and the binding of STAT1 to the GAS
sequence motif in the IRF-1 promoter. The effects of VIP/PACAP are
mediated through the specific VIP/PACAP receptor-1 and the cAMP/protein
kinase A (PKA) transduction pathway, but not through the induction of
suppressor of cytokine signaling-1 or suppressor of cytokine
signaling-3. Because IFN- is a major stimulator of innate immune
responses in vivo, the down-regulation of IFN--induced gene
expression by VIP and PACAP could represent a significant element in
the regulation of the inflammatory response by endogenous
neuropeptides.
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