Linked Life Data

20022349

Source:http://linkedlifedata.com/resource/pubmed/id/20022349

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2010-4-29
pubmed:abstractText
Keratinocytes produce inflammatory mediators that are involved in the pathogenesis of skin disorders such as atopic dermatitis (AD). In particular, the CC chemokines, thymus and activation regulated chemokine (TARC)/CCL17 and mucosae-associated epithelial chemokine (MEC)/CCL28 are considered to play an important role in the lesional infiltration of lymphocytes in canine AD. However, there have been no reports on the regulatory mechanisms of CCL17 and CCL28 transcription in canine keratinocytes. In this study, we investigated whether CCL17 and CCL28 transcription in cultured keratinocytes is induced by TNF-alpha, IL-1beta, or IFN-gamma. It was found that CCL17 mRNA transcription is augmented by TNF-alpha only, whereas the CCL28 mRNA level could be increased by TNF-alpha, IL-1beta, or IFN-gamma. The present study suggests that pro-inflammatory cytokines are important inducing factors for the production of CCL17 and CCL28 in the lesional skin of dogs with AD.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1532-2661
pubmed:author
pubmed:copyrightInfo
Copyright 2009 Elsevier Ltd. All rights reserved.
pubmed:issnType
Electronic
pubmed:volume
88
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
422-6
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Augmentation of CCL17 and CCL28 gene expression by TNF-alpha, IL-1beta, or IFN-gamma in cultured canine keratinocytes.
pubmed:affiliation
The United Graduate School of Veterinary Sciences, Gifu University, 1-1 Yanagido, Gifu 501-1193, Japan. k5104402@edu.gifu-u.ac.jp
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't