Linked Life Data

9606995

Source:http://linkedlifedata.com/resource/pubmed/id/9606995

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1998-6-15
pubmed:abstractText
Recent evidence has demonstrated the importance of substance P and its receptor in macrophage-mediated inflammatory responses. While previous studies have shown that substance P can augment proinflammatory monokine production, little is known about the effects of this neuropeptide on the production of monokines that might limit inflammation. In the present study we have investigated the effect of substance P treatment on the production of transforming growth factor-beta 1 (TGF-beta 1) in cultured murine macrophages. We report that, while substance P agonist alone elicited increases in TGF-beta 1 mRNA expression and modest increases in TGF-beta 1 secretion, substance P dramatically diminished LPS- or IFN-gamma-induced TGF-beta 1 production. These results suggest a previously unrecognized mechanism where substance P may act as a proinflammatory mediator by limiting the production of excessive levels of TGF-beta 1 by LPS- or IFN-gamma-activated macrophages.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0008-8749
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
183
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
113-20
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
Substance P diminishes lipopolysaccharide and interferon-gamma-induced TGF-beta 1 production by cultured murine macrophages.
pubmed:affiliation
Department of Microbiology and Immunology, Tulane University School of Medicine, New Orleans, Louisiana 70112, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.