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Induction of Intracellular Interleukin-1 β Signals via Type II Interleukin-1 Receptor in Human Gingival Fibroblasts

Taipei Medical College

S. Takashiba

Department of Periodontology and Endodontology, Okayama University Dental School, 2-5-1 Shikata-cho, Okayama 700-8525, Japan

H. Maeda

Department of Periodontology and Endodontology, Okayama University Dental School, 2-5-1 Shikata-cho, Okayama 700-8525, Japan

K. Naruishi

Department of Periodontology and Endodontology, Okayama University Dental School, 2-5-1 Shikata-cho, Okayama 700-8525, Japan

F. Nishimura

Department of Periodontology and Endodontology, Okayama University Dental School, 2-5-1 Shikata-cho, Okayama 700-8525, Japan

H. Arai

Department of Periodontology and Endodontology, Okayama University Dental School, 2-5-1 Shikata-cho, Okayama 700-8525, Japan

H.-k. Lu

Taipei Medical College School of Dentistry, 250 Wu-Shing Street, Taipei, Taiwan, ROC

Y. Murayama

Department of Periodontology and Endodontology, Okayama University Dental School, 2-5-1 Shikata-cho, Okayama 700-8525, Japan, murayama{at}dent.okayama-u.ac.jp

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.

Key Words: interleukin-1β (IL-1) • type II IL-1 receptor (IL-1RII) • cytokine gene expression • signaling • human gingival fibroblasts.

Journal of Dental Research, Vol. 79, No. 9, 1683-1688 (2000)
DOI: 10.1177/00220345000790090801


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