Epidermal growth factor synergistically enhances interleukin-8 production in human gingival fibroblasts stimulated with interleukin-1β

被引:18
作者
Yucel-Lindberg, Tulay [1 ]
Brunius, Gustaf [1 ]
机构
[1] Karolinska Inst, Inst Odontol, Dept Pediat Dent, SE-14104 Huddinge, Sweden
关键词
epidermal growth factor; interleukin-8; interleukin-1; beta; gingival fibroblasts; tyrosine kinase; p38 MAP kinase;
D O I
10.1016/j.archoralbio.2006.03.004
中图分类号
R78 [口腔科学];
学科分类号
1003 ;
摘要
The chemokine interleukin-8 (IL-8) has been implicated in inflammatory diseases including periodontitis. In this study the effect of epidermal growth factor (EGF) on the production and regulation of interteukin-8 (IL-8) in human gingival fibroblasts challenged with interleukin-1 beta (IL-1 beta) was investigated. EGF, in comparison to the effect of IL-1 beta, weakly increased the mRNA and protein expression of IL-8 in gingival fibroblasts. When the cells were treated simultaneously with EGF and IL-1 beta, however, EGF synergistically enhanced them RNA expression and production of IL-8. The stimulatory effect of EGF on IL-1 beta-induced IL-8 production was completely abolished by the broad range tyrosine kinase inhibitor Herbimycin A, and considerably reduced by the receptor tyrosine kinase specific inhibitor PD 153035. Herbimycin A abolished IL-8 production induced by IL-1 beta, whereas PD 153035 had no effect on the cytokine-induced IL-8 production. Furthermore, the p38 mitogen-activated protein (MAP) kinase inhibitor SB 203580 reduced IL-8 production induced by IL-1 beta as well as by the combination of EGF and IL-1 beta but had no effect on EGF-induced IL-8 production. In conclusion, the study demonstrates that EGF synergistically stimulates IL-8 production in the presence of IL-1 beta and that tyrosine kinase(s) seem to be involved in the signalling pathway of IL-1 beta and EGF. The synergistic interactions between EGF and IL-1 beta on IL-8 production may play an essential rote in the pathogenesis of the inflammatory disease periodontitis. (c) 2006 Elsevier Ltd. All rights reserved.
引用
收藏
页码:892 / 898
页数:7
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