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*
Department of Biological Sciences, Rutgers University, Newark, NJ 07102; and
Departamento Biologia Celular, Universidad Complutense, Madrid, Spain
Vasoactive intestinal peptide (VIP), a neuropeptide present in the
lymphoid microenvironment, and the structurally related pituitary
adenylate cyclase-activating polypeptide (PACAP) act as potent
anti-inflammatory agents that inhibit the function of activated
macrophages and TH cells. Previous reports showed that VIP/PACAP
inhibit IL-6 and TNF-
production in LPS-stimulated macrophages. The
present study reports on the effect of VIP/PACAP on IL-10 production.
Although VIP/PACAP do not induce IL-10 by themselves, they enhance
IL-10 production in LPS-stimulated macrophages. The specific VPAC1
receptor mediates the stimulatory effect of VIP/PACAP, and cAMP is the
major second messenger involved. VIP/PACAP increase IL-10 mRNA in
LPS-stimulated cells, and the effect of transcriptional and protein
synthesis inhibitors indicates de novo IL-10 production.
Electromobility shift assays show that VIP/PACAP induce an increase in
nuclear cAMP response element (CRE)-binding complexes, with CRE binding
protein as the major active component. Treatments with either a VPAC1
antagonist or a protein kinase A inhibitor abolish IL-10 stimulation
and, concomitantly, the increase in CRE binding. Effects similar to the
in vitro stimulation of IL-10 were obtained in vivo in mice treated
with LPS and VIP or PACAP. The neuropeptides induce increased levels of
IL-10 in both serum and peritoneal fluid, and increased expression of
the IL-10 mRNA in peritoneal exudate cells. The stimulation of IL-10
production in activated macrophages represents a novel
anti-inflammatory activity of VIP and PACAP, which presumably acts
in vivo in conjunction with the inhibition of proinflammatory cytokines
such as IL-6 and TNF- to reduce the magnitude of the immune
response.
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