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

H. H. Chou, S. Takashiba, H. Maeda, K. Naruishi, F. Nishimura, H. Arai, H. K. Lu, Y. Murayama

研究成果: 雜誌貢獻文章

14 引文 (Scopus)

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-1β mRNA and IL-6 mRNA in response to IL-1β 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-1β 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-1β stimulation, possibly by altering the IL-1RI-dependent signals.
原文英語
頁(從 - 到)1683-1688
頁數6
期刊Journal of Dental Research
79
發行號9
出版狀態已發佈 - 2000

指紋

Interleukin-1
Fibroblasts
Messenger RNA
Cytokines
Interleukin-1 Type II Receptors
Phosphorylation
Interleukin-1 Receptors
Periodontal Diseases
Amino Acid Substitution
human IL1R2 protein
Neutralizing Antibodies
Interleukin-8
Connective Tissue
Organism Cloning
Interleukin-6
Proteins
B-Lymphocytes
Complementary DNA
Inflammation
Cell Line

ASJC Scopus subject areas

  • Dentistry(all)

引用此文

Chou, H. H., Takashiba, S., Maeda, H., Naruishi, K., Nishimura, F., Arai, H., ... Murayama, Y. (2000). Induction of intracellular interleukin-1β signals via type II interleukin-1 receptor in human gingival fibroblasts. Journal of Dental Research, 79(9), 1683-1688.

Induction of intracellular interleukin-1β signals via type II interleukin-1 receptor in human gingival fibroblasts. / Chou, H. H.; Takashiba, S.; Maeda, H.; Naruishi, K.; Nishimura, F.; Arai, H.; Lu, H. K.; Murayama, Y.

於: Journal of Dental Research, 卷 79, 編號 9, 2000, p. 1683-1688.

研究成果: 雜誌貢獻文章

Chou, HH, Takashiba, S, Maeda, H, Naruishi, K, Nishimura, F, Arai, H, Lu, HK & Murayama, Y 2000, 'Induction of intracellular interleukin-1β signals via type II interleukin-1 receptor in human gingival fibroblasts', Journal of Dental Research, 卷 79, 編號 9, 頁 1683-1688.
Chou, H. H. ; Takashiba, S. ; Maeda, H. ; Naruishi, K. ; Nishimura, F. ; Arai, H. ; Lu, H. K. ; Murayama, Y. / Induction of intracellular interleukin-1β signals via type II interleukin-1 receptor in human gingival fibroblasts. 於: Journal of Dental Research. 2000 ; 卷 79, 編號 9. 頁 1683-1688.
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abstract = "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-1β mRNA and IL-6 mRNA in response to IL-1β 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-1β 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-1β stimulation, possibly by altering the IL-1RI-dependent signals.",
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AU - Chou, H. H.

AU - Takashiba, S.

AU - Maeda, H.

AU - Naruishi, K.

AU - Nishimura, F.

AU - Arai, H.

AU - Lu, H. K.

AU - Murayama, Y.

PY - 2000

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N2 - 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-1β mRNA and IL-6 mRNA in response to IL-1β 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-1β 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-1β stimulation, possibly by altering the IL-1RI-dependent signals.

AB - 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-1β mRNA and IL-6 mRNA in response to IL-1β 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-1β 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-1β stimulation, possibly by altering the IL-1RI-dependent signals.

KW - Cytokine gene expression

KW - Human gingival fibroblasts

KW - Interleukin-1β (IL-1)

KW - Signaling

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