Source:http://linkedlifedata.com/resource/pubmed/id/10326728
Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
|
pubmed:dateCreated |
1999-5-26
|
pubmed:abstractText |
Interleukin-1 (IL-1) may play a critical role in immune and inflammatory responses in inflamed gingiva, and it is synthesized by a wide variety of host cells. In this study, we examined the regulatory effects of various cytokines on bioactive membrane IL-1 and intracellular IL-1 alpha production in cultured human gingival fibroblasts (HGF). Recombinant human (rh) IL-1 beta stimulated membrane IL-1 activity, which was mainly attributed to IL-1 alpha. rhIL-1 beta and rh tumor necrosis factor (TNF)-alpha stimulated HGF to produce intracellular IL-1 alpha, whereas rh interleukin-6 (IL-6), rh interleukin-4 (IL-4), and rh interferon (IFN)-gamma did not do so. Intracellular IL-1 alpha production induced by rhIL-1 beta or rhTNF-alpha may be partially related to protein kinase C (PKC) activation, because rhIL-1 beta or rhTNF-alpha-induced intracellular IL-1 alpha production was stimulated by pre-treatment with 12-o-tetradecanoylphorbol 13-acetate (TPA), a PKC activator, but was suppressed by the pre-treatment with 1-(5-isoquinoline-sulfonyl) -2-methylpiperazine dihydrochloride (H-7), which is a PKC inhibitor. rhIL-4 inhibited rhIL-1 beta- or rhTNF-alpha-induced intracellular IL-1 alpha production, but rhIL-6 had no effect on this production. Pre-treatment with rh IFN-gamma remarkably enhanced intracellular IL-1 alpha production induced by subsequent treatment with rhIL-1 beta or rhTNF-alpha. Simultaneous treatment with rhIFN-gamma and rhIL-1 beta inhibited rhIL-1 beta-induced intracellular IL-1 alpha production, but co-treatment with rhIFN-gamma and rhTNF-alpha enhanced rhTNF-alpha-induced intracellular IL-1 alpha production. These results suggest that in inflamed gingiva, pro-inflammatory cytokines such as IL-1 beta and TNF-alpha may induce bioactive intracellular IL-1 alpha production in human gingival fibroblasts and that this production can be differentially modulated by T-cell-derived cytokines such as IFN-gamma or IL4.
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
D
|
pubmed:chemical | |
pubmed:status |
MEDLINE
|
pubmed:month |
Apr
|
pubmed:issn |
0022-0345
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:volume |
78
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
840-9
|
pubmed:dateRevised |
2006-11-15
|
pubmed:meshHeading |
pubmed-meshheading:10326728-Adult,
pubmed-meshheading:10326728-Analysis of Variance,
pubmed-meshheading:10326728-Cells, Cultured,
pubmed-meshheading:10326728-Cytokines,
pubmed-meshheading:10326728-Dose-Response Relationship, Drug,
pubmed-meshheading:10326728-Fibroblasts,
pubmed-meshheading:10326728-Gingiva,
pubmed-meshheading:10326728-Humans,
pubmed-meshheading:10326728-Interleukin-1,
pubmed-meshheading:10326728-Recombinant Proteins,
pubmed-meshheading:10326728-Time Factors
|
pubmed:year |
1999
|
pubmed:articleTitle |
Intracellular interleukin-1 alpha production in human gingival fibroblasts is differentially regulated by various cytokines.
|
pubmed:affiliation |
Department of Periodontics, Showa University Dental School, Tokyo, Japan.
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|