Linked Life Data

7583353

Source:http://linkedlifedata.com/resource/pubmed/id/7583353

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1995-11-30
pubmed:abstractText
Lipopolysaccharide (LPS) stimulation of the human monocytic cell line Mono Mac 6 leads to rapid expression of both the pro-inflammatory cytokine tumor necrosis factor (TNF) and the anti-inflammatory cytokine interleukin-10 (IL-10). Preculture of these cells with a low dose of LPS for 2 days rendered the cells tolerant to subsequent stimulation, in that TNF gene expression is only minimal, both at the mRNA and at the protein level. IL-10 shows a reciprocal pattern, however, as expression of this gene is upregulated in precultured cells, and it will further increase upon subsequent stimulation. Although TNF has been shown to induce IL-10, and IL-10 was found to downregulate TNF, this reciprocal regulation does not explain the pattern observed in LPS tolerance in Mono Mac 6, since neutralizing antibodies against TNF and IL-10 could not prevent upregulation of IL-10 and downregulation of TNF, respectively. Treatment of Mono Mac 6 cells during LPS preculture with interferon-gamma (IFN-gamma) could, however, reverse tolerance: LPS/IFN-gamma precultured cells produced high levels of TNF transcripts upon subsequent stimulation, while the response of the IL-10 gene was attenuated. The data show that LPS tolerance does not involve a passive downregulation of all types of monocyte functions, but it is an orchestrated response with downregulation of pro- and upregulation of anti-inflammatory cytokines.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1078-7852
pubmed:author
pubmed:issnType
Print
pubmed:volume
45
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
56-63
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
Interleukin-10 is upregulated in LPS tolerance.
pubmed:affiliation
Institute for Immunology, University of Munich, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't