Linked Life Data

7511596

Source:http://linkedlifedata.com/resource/pubmed/id/7511596

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
13
pubmed:dateCreated
1994-5-5
pubmed:abstractText
The regulation of interleukin (IL)-6 synthesis by cAMP-increasing agents remains an unresolved issue. Since an increase in cAMP levels via activation of histamine H2 receptors does not induce IL-1 beta synthesis but enhances self-induction of IL-1 (Vannier, E., and Dinarello, C. A. (1993) J. Clin. Invest. 92, 281-287), we investigated whether histamine regulates IL-6 synthesis. Human peripheral blood mononuclear cells were stimulated with IL-1 alpha in the absence or presence of histamine (1 nM to 100 microM). IL-6 was measured using a specific radioimmunoassay. Histamine alone did not induce protein synthesis or mRNA accumulation for IL-6. Histamine (1-100 microM) enhanced IL-1 alpha-induced synthesis of IL-6 (p < 0.001). Cimetidine and ranitidine, H2 receptor antagonists structurally unrelated to each other, completely reversed the histamine-mediated increase in IL-1 alpha-induced IL-6 synthesis. However, diphenhydramine, an H1 receptor antagonist, did not reverse this effect. Prostaglandin E2, an activator of adenylate cyclase, also enhanced IL-1 alpha-induced synthesis of IL-6. Histamine increased and sustained steady-state levels of IL-6 mRNA in IL-1 alpha-stimulated cells, but reduced IL-6 mRNA half-life (3.5 h versus 1.8 h). Our results indicate that cAMP-increasing agents, such as histamine or prostaglandin E2, fail to induce IL-6 synthesis but rather enhance IL-1-induced IL-6 synthesis.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
269
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
9952-6
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
Histamine enhances interleukin (IL)-1-induced IL-6 gene expression and protein synthesis via H2 receptors in peripheral blood mononuclear cells.
pubmed:affiliation
Department of Medicine, Tufts University School of Medicine, Boston, Massachusetts.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.