Linked Life Data

21176858

Source:http://linkedlifedata.com/resource/pubmed/id/21176858

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2011-5-6
pubmed:abstractText
PGlyRPs recognize bacterial peptidoglycan and function in antibacterial innate immunity. Focusing on the interference between nutrition and recognition pattern proteins, free fatty acids (FFA) of dietary and bacterial sources may exert their immunological response through modulating the expression level of the PGlyRPs in enterocytes. PGlyRP3 was the only PGlyRPs member expressed in Caco2 cells. In silico analysis showed that the promoter of PGlyRP3 has some PPRE regions that, as tested by EMSA, bind physically to the PPAR?-RXR? complex. PGlyRP3 gene expression was induced by PPAR? ligands including GW1929 and some FFA. Overexpression of PGlyRP3 in Caco2 cells down regulated the expression of the inflammatory cytokines IL-8, IL-12 and TNF-?, while its silencing increased the expression of these cytokines. FFA that induced the PGlyRP3 inhibited the tested cytokines. Silencing of PGlyRP3 gene caused the same FFA to increase the cytokine gene expression. A negative regulation of NF-?B pathway, including up-regulation of I??-? and down regulation of NF-?B and COX-2, is involved in the anti-inflammatory effects of PGlyRP3. In conclusion, PPAR? mediates a modulation of PGlyRP3 gene expression, which is involved in inhibiting inflammation through negative regulation of NF-?B pathway.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1878-3279
pubmed:author
pubmed:copyrightInfo
Copyright © 2010 Elsevier GmbH. All rights reserved.
pubmed:issnType
Electronic
pubmed:volume
216
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
715-24
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
PPAR?-dependent peptidoglycan recognition protein 3 (PGlyRP3) expression regulates proinflammatory cytokines by microbial and dietary fatty acids.
pubmed:affiliation
Department of Physiology and Biochemistry of Nutrition, Max Rubner Institute, Hermann Weigmann Str. 1, 24103 Kiel, Germany. zenhomm@scientist.com
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't