Linked Life Data

9973516

Source:http://linkedlifedata.com/resource/pubmed/id/9973516

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1999-4-13
pubmed:abstractText
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-alpha 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-alpha by endotoxin-activated murine peritoneal macrophages. Both neuropeptides rapidly and specifically inhibit the LPS-stimulated production of TNF-alpha, 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-alpha at a transcriptional level. In vitro results were correlated with an inhibition of both TNF-alpha 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-alpha, IL-1beta, 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-alpha to reduce inflammation or shock.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
162
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2358-67
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:9973516-Animals, pubmed-meshheading:9973516-Cells, Cultured, pubmed-meshheading:9973516-Cytokines, pubmed-meshheading:9973516-Female, pubmed-meshheading:9973516-Inflammation, pubmed-meshheading:9973516-Injections, Intraperitoneal, pubmed-meshheading:9973516-Intracellular Fluid, pubmed-meshheading:9973516-Lipopolysaccharides, pubmed-meshheading:9973516-Macrophages, Peritoneal, pubmed-meshheading:9973516-Mice, pubmed-meshheading:9973516-Mice, Inbred BALB C, pubmed-meshheading:9973516-Neuropeptides, pubmed-meshheading:9973516-Pituitary Adenylate Cyclase-Activating Polypeptide, pubmed-meshheading:9973516-RNA, Messenger, pubmed-meshheading:9973516-Signal Transduction, pubmed-meshheading:9973516-Time Factors, pubmed-meshheading:9973516-Tumor Necrosis Factor-alpha, pubmed-meshheading:9973516-Vasoactive Intestinal Peptide
pubmed:year
1999
pubmed:articleTitle
Vasoactive intestinal peptide and pituitary adenylate cyclase-activating polypeptide inhibit endotoxin-induced TNF-alpha production by macrophages: in vitro and in vivo studies.
pubmed:affiliation
Department of Cellular Biology, Faculty of Biology, Complutense University, Madrid, Spain.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't