Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2010-4-5
pubmed:abstractText
B lymphocyte stimulator (BLyS), B cell activating factor (BAFF), a member of the tumor necrosis factor ligand superfamily has potent co-stimulatory activity on B cells, and BLyS-production in the airway mucosa is of potential importance as it triggers innate and adaptive immune responses. To investigate whether airway fibroblast could express BLyS, we examined BLyS-expression in human nasal airway fibroblasts and compared to its expression in tonsillar and skin fibroblasts as well as the effect of the Toll-like receptor (TLR) ligands on that in human nasal airway fibroblasts. The expression of BLyS by nasal fibroblasts in the presence of polyinocinic-polycytidykic acid (poly(I:C)) was markedly induced, to a level of more than 100 times higher than that observed in the absence of poly(I:C). In order to demonstrate the intracellular pathways involved in poly(I:C)-induced BLyS-expression, we used specific inhibitors of phosphatidylinositol 3-kinase (PI3-kinase), spleen tyrosine kinase (Syk), p38 mitogen-activated protein kinase (p38 MAPK), c-Jun N-terminal kinase (JNK), and extracellular-signal related kinase (ERK)-signaling in these events. Pre-incubation with the PI3-kinase inhibitor LY294002 or Wortmanin reversed the poly(I:C)-induced production and expression of BLyS. Syk kinase inhibitor Piceatannol partially reduced its production and expression. Thus, we were able to show that PI3-kinase signaling is directly involved in poly(I:C)-induced BLyS-expression in nasal airway fibroblasts. These results indicate that human nasal airway fibroblasts strongly induce BLyS-expression and production by poly(I:C) through PI3-K signaling during airway immune responses.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1096-0023
pubmed:author
pubmed:copyrightInfo
Crown Copyright (c) 2010. Published by Elsevier Ltd. All rights reserved.
pubmed:issnType
Electronic
pubmed:volume
50
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
163-9
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:20089415-Adult, pubmed-meshheading:20089415-B-Cell Activating Factor, pubmed-meshheading:20089415-Cells, Cultured, pubmed-meshheading:20089415-Dose-Response Relationship, Drug, pubmed-meshheading:20089415-Female, pubmed-meshheading:20089415-Fibroblasts, pubmed-meshheading:20089415-Gene Expression Regulation, pubmed-meshheading:20089415-Humans, pubmed-meshheading:20089415-Ligands, pubmed-meshheading:20089415-Male, pubmed-meshheading:20089415-Nose, pubmed-meshheading:20089415-Phosphatidylinositol 3-Kinases, pubmed-meshheading:20089415-Poly I-C, pubmed-meshheading:20089415-Protein Kinase Inhibitors, pubmed-meshheading:20089415-RNA, Messenger, pubmed-meshheading:20089415-Signal Transduction, pubmed-meshheading:20089415-Time Factors, pubmed-meshheading:20089415-Toll-Like Receptors
pubmed:year
2010
pubmed:articleTitle
Poly(I:C) induces BLyS-expression of airway fibroblasts through phosphatidylinositol 3-kinase.
pubmed:affiliation
Department of Otorhinolaryngology, University of Fukui, 23-3 Matsuoka-Shimoaizuki, Eiheiji, Yoshida, Fukui, Japan. ymdtkcy@u-fukui.ac.jp
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't