Induction of intracellular interleukin-1β signals via type II interleukin-1 receptor in human gingival fibroblasts

被引:12
作者
Chou, HH
Takashiba, S
Maeda, H
Naruishi, K
Nishimura, F
Arai, H
Lu, H
Murayama, Y
机构
[1] Okayama Univ, Sch Dent, Dept Periodontol & Endodontol, Okayama 7008525, Japan
[2] Taipei Med Coll, Sch Dent, Taipei, Taiwan
关键词
interleukin-1 beta (IL-1); type IIIL-1 receptor (IL-1RII); cytokine gene expression; signaling; human gingival fibroblasts;
D O I
10.1177/00220345000790090801
中图分类号
R78 [口腔科学];
学科分类号
1003 ;
摘要
The type II interleukin-1 receptor (IL-1RII) has been thought to be incapable of transducing signals to cells because of its short intracellular domain, while type I IL-1 receptor (IL-1RI) does transduce signals. Since over-expression of IL-1RII has been demonstrated to inhibit cytokine production in the fibroblastic cell line, it has been proposed to use IL-1RII to prevent IL-1-induced inflammation in connective tissue. In this study, trace amounts of IL-1RII mRNA expression were detected in human gingival fibroblasts (HGFs), which are affected by cytokines in inflammatory periodontal disease. Cloning of the cDNA encoding IL-1RII expressed in HGFs revealed 3 amino acid substitutions in the extracellular domain, when compared with the 408 residues predicted from human B-cells. Over-expression of IL-1RII on HGFs by gene transfer down-regulated the expression of IL-1 beta mRNA and IL-6 mRNA in response to IL-1 beta stimulation, while the expression of IL-8 mRNA was not affected. In the IL-1RII-transfected HGFs, phosphorylation of 25- and 74-kDa proteins was up-regulated upon IL-1 beta stimulation in the transfected HGFs. The phosphorylation of these proteins was suppressed by the addition of a neutralizing antibody against IL-1RII. These results suggest that the IL-1RII may regulate HGFs expression of cytokine mRNA upon IL-1 beta stimulation, possibly by altering the IL-1RI-dependent signals.
引用
收藏
页码:1683 / 1688
页数:6
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