Linked Life Data

15598438

Source:http://linkedlifedata.com/resource/pubmed/id/15598438

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2004-12-15
pubmed:abstractText
CTACK/CCL27 is pivotal in mediating the migration of lymphocytes into the skin, through the binding to the chemokine receptor CCR10. CCL27 is continuously expressed by keratinocytes, but highly upregulated in inflammatory skin diseases such as atopic dermatitis and psoriasis. CCL27 can be induced in cultured keratinocytes by tumor necrosis factor (TNF)-alpha, which is also known to induce activity of the transcription factor NF-kappaB. NF-kappaB plays a vital role in controlling inflammation through its regulation of transcription of chemokines and pro-inflammatory cytokines. We show here that inhibition of NF-kappaB with the non-specific NF-kappaB inhibitors SSC (sodium salicylate), DCIC (3,4-dichloroisocoumarin) and PAO (phenylarsine oxide) results in a downregulation of TNF-alpha-induced CCL27 production. To substantiate the result and to investigate the role of NF-kappaB we investigated if specific antisense oligonucleotides against the p50 and p65 subunits of NF-kappaB had the same effect. Inhibition of either p50 or p65 production with antisense oligonucleotides resulted in a significant downregulation of TNF-alpha-induced CCL27 production. These results indicate that CCL27 expression is under the control of NF-kappaB, and that NF-kappaB, as indicated by others, may be an attractive target for therapy in inflammatory skin diseases.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1043-4666
pubmed:author
pubmed:issnType
Print
pubmed:day
21
pubmed:volume
29
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
49-55
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
Tumor necrosis factor-alpha-induced CTACK/CCL27 (cutaneous T-cell-attracting chemokine) production in keratinocytes is controlled by nuclear factor kappaB.
pubmed:affiliation
Department of Dermatology, Research Laboratory D, Marselisborg Centret, Aarhus Amtssygehus, University of Aarhus, PP Ørumsgade 11, DK 8000 Aarhus C, Denmark. chr-vest@post9.tele.dk
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't