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Production by Macrophages: In Vitro and In Vivo Studies1
*
Department of Cellular Biology, Faculty of Biology, Complutense University, Madrid, Spain;
Department of Medical Biochemistry and Molecular Biology, University of Seville School of Medicine and Virgen Macarena Hospital, Seville, Spain; and
Department of Biological Sciences, Rutgers University, Newark, NJ 07102
Vasoactive intestinal peptide (VIP) is a neuropeptide synthesized
by immune cells that can modulate several immune aspects, including the
function of cells involved in the inflammatory response, such as
macrophages and monocytes. The production and release of cytokines by
activated phagocytes are important events in the pathogenesis of
ischemia-reperfusion injury. There is abundant evidence that the
proinflammatory cytokine TNF-
is an important mediator of shock and
organ failure complicating Gram-negative sepsis. VIP has been shown to
attenuate the deleterious consequences of this pathologic phenomenon.
In this study we have investigated the effects of VIP and the
structurally related neuropeptide pituitary adenylate
cyclase-activating polypeptide (PACAP38) on the production of TNF-
by endotoxin-activated murine peritoneal macrophages. Both
neuropeptides rapidly and specifically inhibit the LPS-stimulated
production of TNF-, exerting their action through the binding to
VPAC1 receptor and the subsequent activation of the adenylate cyclase
system. VIP and PACAP regulate the production of TNF- at a
transcriptional level. In vitro results were correlated with an
inhibition of both TNF- expression and release in endotoxemic mice
in vivo. The immunomodulatory role of VIP in vivo is supported by the
up-regulation of VIP release in serum and peritoneal fluid by LPS and
proinflammatory cytokines such as TNF-, IL-1ß, and IL-6. These
findings support the idea that under toxicity conditions associated
with high LPS doses, VIP and PACAP could act as protective mediators
that regulate the excessive release of TNF- to reduce inflammation
or shock.
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