Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2004-10-20
pubmed:abstractText
The intestinal epithelium serves as a barrier to the intestinal flora. In response to pathogens, intestinal epithelial cells (IEC) secrete proinflammatory cytokines. To aid in defense against bacteria, IEC also secrete antimicrobial peptides, termed defensins. The aim of our studies was to understand the role of TLR signaling in regulation of beta-defensin expression by IEC. The effect of LPS and peptidoglycan on beta-defensin-2 expression was examined in IEC lines constitutively or transgenically expressing TLRs. Regulation of beta-defensin-2 was assessed using promoter-reporter constructs of the human beta-defensin-2 gene. LPS and peptidoglycan stimulated beta-defensin-2 promoter activation in a TLR4- and TLR2-dependent manner, respectively. A mutation in the NF-kappaB or AP-1 site within the beta-defensin-2 promoter abrogated this response. In addition, inhibition of Jun kinase prevents up-regulation of beta-defensin-2 protein expression in response to LPS. IEC respond to pathogen-associated molecular patterns with expression of the antimicrobial peptide beta-defensin-2. This mechanism may protect the intestinal epithelium from pathogen invasion and from potential invaders among the commensal flora.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Surface, http://linkedlifedata.com/resource/pubmed/chemical/DEFB4A protein, human, http://linkedlifedata.com/resource/pubmed/chemical/LY96 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Lipopolysaccharides, http://linkedlifedata.com/resource/pubmed/chemical/Lymphocyte Antigen 96, http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins, http://linkedlifedata.com/resource/pubmed/chemical/Peptidoglycan, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cell Surface, http://linkedlifedata.com/resource/pubmed/chemical/TLR2 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/TLR4 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/TLR6 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Tlr6 protein, mouse, http://linkedlifedata.com/resource/pubmed/chemical/Toll-Like Receptor 2, http://linkedlifedata.com/resource/pubmed/chemical/Toll-Like Receptor 4, http://linkedlifedata.com/resource/pubmed/chemical/Toll-Like Receptor 6, http://linkedlifedata.com/resource/pubmed/chemical/Toll-Like Receptors, http://linkedlifedata.com/resource/pubmed/chemical/beta-Defensins
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
173
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5398-405
pubmed:dateRevised
2010-9-17
pubmed:meshHeading
pubmed-meshheading:15494486-Animals, pubmed-meshheading:15494486-Antigens, Surface, pubmed-meshheading:15494486-Caco-2 Cells, pubmed-meshheading:15494486-Cell Line, pubmed-meshheading:15494486-Cell Line, Tumor, pubmed-meshheading:15494486-Humans, pubmed-meshheading:15494486-Intestinal Mucosa, pubmed-meshheading:15494486-Lipopolysaccharides, pubmed-meshheading:15494486-Lymphocyte Antigen 96, pubmed-meshheading:15494486-Membrane Glycoproteins, pubmed-meshheading:15494486-Mice, pubmed-meshheading:15494486-Peptidoglycan, pubmed-meshheading:15494486-Receptors, Cell Surface, pubmed-meshheading:15494486-Signal Transduction, pubmed-meshheading:15494486-Toll-Like Receptor 2, pubmed-meshheading:15494486-Toll-Like Receptor 4, pubmed-meshheading:15494486-Toll-Like Receptor 6, pubmed-meshheading:15494486-Toll-Like Receptors, pubmed-meshheading:15494486-Up-Regulation, pubmed-meshheading:15494486-beta-Defensins
pubmed:year
2004
pubmed:articleTitle
Beta-defensin-2 expression is regulated by TLR signaling in intestinal epithelial cells.
pubmed:affiliation
Inflammatory Bowel Disease Center, Division of Gastroenterology, Department of Medicine, Mount Sinai School of Medicine, New York, NY 10029, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.