Linked Life Data

11342660

Source:http://linkedlifedata.com/resource/pubmed/id/11342660

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2001-5-8
pubmed:abstractText
The murine calcium binding protein S100A8 (A8) is a leukocyte chemoattractant, but high levels may be protective and scavenge hypochlorite. A8 is induced by LPS, IFN-gamma, and TNF in elicited macrophages. Th2 cytokines generally suppress proinflammatory gene expression, and IL-4 and IL-13 partially decreased A8 induction in macrophages and endothelial cells stimulated by LPS or IFN. In contrast, IL-10 synergized with LPS and IFN to increase mRNA levels > or =9-fold and secreted A8 levels approximately 4-fold. IL-10 decreased the optimal time of mRNA expression induced by LPS from 24 to 8 h. Blocking experiments indicated that endogenous IL-10 contributes to gene induction by LPS. Cooperation between IL-10 and LPS was not due to altered mRNA stability but was dependent on de novo protein synthesis. Transfection analysis with A8 luciferase constructs confirmed that synergy was due to increased transcription. The region of the promoter involved was localized to a 178-bp fragment flanking the transcription start site of the gene. This region was also responsible for the suppressive effects of IL-4 and IL-13. Forskolin, CTP-cAMP, and PGE(2) also enhanced LPS- and IFN-induced A8 mRNA, whereas indomethacin significantly reduced synergy between IL-10 and LPS. Mitogen-activated protein kinase/cyclooxygenase 2/cAMP pathways involving CCAAT-enhancing binding protein, located within the active promoter, may mediate A8 gene up-regulation in a manner mechanistically distinct to genes regulated by IL-10 via the STAT pathway. A8 exhibits pleiotropic effects, and the high levels secreted as a result of IL-10 synergy may regulate untoward inflammatory damage by virtue of its an antioxidant capacity.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
166
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
6358-66
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:11342660-Adjuvants, Immunologic, pubmed-meshheading:11342660-Animals, pubmed-meshheading:11342660-Antigens, Differentiation, pubmed-meshheading:11342660-Calcium-Binding Proteins, pubmed-meshheading:11342660-Calgranulin A, pubmed-meshheading:11342660-Cells, Cultured, pubmed-meshheading:11342660-Cyclic AMP, pubmed-meshheading:11342660-Dinoprostone, pubmed-meshheading:11342660-Down-Regulation, pubmed-meshheading:11342660-Drug Synergism, pubmed-meshheading:11342660-Gene Expression Regulation, pubmed-meshheading:11342660-Interleukin-10, pubmed-meshheading:11342660-Interleukin-13, pubmed-meshheading:11342660-Interleukin-4, pubmed-meshheading:11342660-Macrophages, pubmed-meshheading:11342660-Mice, pubmed-meshheading:11342660-RNA, Messenger, pubmed-meshheading:11342660-Transcriptional Activation, pubmed-meshheading:11342660-Transforming Growth Factor beta, pubmed-meshheading:11342660-Up-Regulation
pubmed:year
2001
pubmed:articleTitle
Il-10 up-regulates macrophage expression of the S100 protein S100A8.
pubmed:affiliation
Cytokine Research Unit, School of Pathology, Faculty of Medicine, University of New South Wales, Sydney, Australia.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't