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Research ArticleINFLAMMATION AND IMMUNOPHARMACOLOGY

Effect of β2-Adrenergic Receptor Stimulation on Interleukin-18-Induced Intercellular Adhesion Molecule-1 Expression and Cytokine Production

Hideo Kohka Takahashi, Toshihiko Morichika, Hiromi Iwagaki, Tadashi Yoshino, Ryuji Tamura, Shinnya Saito, Shuji Mori, Tadaatsu Akagi, Noriaki Tanaka and Masahiro Nishibori
Journal of Pharmacology and Experimental Therapeutics February 2003, 304 (2) 634-642; DOI: https://doi.org/10.1124/jpet.102.042622
Hideo Kohka Takahashi
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Toshihiko Morichika
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Hiromi Iwagaki
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Tadashi Yoshino
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Ryuji Tamura
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Shinnya Saito
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Shuji Mori
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Tadaatsu Akagi
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Noriaki Tanaka
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Masahiro Nishibori
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Abstract

β-Adrenergic receptor (AR) agonists have been demonstrated to modulate the production of inflammatory mediators. Recent studies implied that β2-AR agonists might be useful for chronic inflammatory diseases caused by interleukin (IL)-18. In the present study, we found that norepinephrine, epinephrine, or isoproterenol down-regulated IL-18 (100 ng/ml)-induced intercellular adhesion molecule (ICAM)-1 expression on monocytes in a dose-dependent manner (10−8–10−4 M), but did not effect B7.1 and B7.2 expression after 24-h incubation. The modulatory effect of these catecholamines on ICAM-1 expression was antagonized by β2-AR antagonist, but not by α1-, α2-, or β1-AR antagonist. β2-AR-selective agonists salbutanol and terbutaline down-regulated IL-18-induced ICAM-1 expression on monocytes, but α1-, α2-, or β1-AR agonist had no effect. In the same manner, salbutanol and terbutaline as well as norepinephrine, epinephrine, and isoproterenol regulated the IL-18-induced cytokine production, including IL-12, tumor necrosis factor-α or interferon-γ through the stimulation of β2-AR. Together with the previous finding that ICAM-1/lymphocyte function-associated antigen-1 interaction plays a crucial role in the IL-18-initiated cytokine network, the present study strongly suggested that the stimulation of β2-AR inhibited the IL-18-activated cytokine cascade through the inhibitory effect on ICAM-1 expression, contributing to finding a new method for clinical treatment.

Footnotes

  • This study was supported in part by a grant from Japan Society for Promotion of Science (BSAR-521/0003815; to M.N.), grants for promotion of research from Okayama University (21, to M.N.; 26, to T.A.), and a grant from the Okayama Medical Foundation (to H.K.T.).

  • DOI: 10.1124/jpet.102.042622

  • Abbreviations:
    IL
    interleukin
    Th
    T helper
    NK
    natural killer
    IFN
    interferon
    ICAM
    intercellular adhesion molecule
    AR
    adrenergic receptor
    MS
    multiple sclerosis
    RA
    rheumatoid arthritis
    LFA
    lymphocyte function-associated antigen
    PBMC
    peripheral blood mononuclear cell
    FITC
    fluorescein isothiocyanate
    mAb
    monoclonal antibody
    CMC
    class-matched control
    Ab
    antibody
    TNF
    tumor necrosis factor
    ELISA
    enzyme-linked immunosorbent assay
    • Received August 6, 2002.
    • Accepted October 30, 2002.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics: 304 (2)
Journal of Pharmacology and Experimental Therapeutics
Vol. 304, Issue 2
1 Feb 2003
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Research ArticleINFLAMMATION AND IMMUNOPHARMACOLOGY

Effect of β2-Adrenergic Receptor Stimulation on Interleukin-18-Induced Intercellular Adhesion Molecule-1 Expression and Cytokine Production

Hideo Kohka Takahashi, Toshihiko Morichika, Hiromi Iwagaki, Tadashi Yoshino, Ryuji Tamura, Shinnya Saito, Shuji Mori, Tadaatsu Akagi, Noriaki Tanaka and Masahiro Nishibori
Journal of Pharmacology and Experimental Therapeutics February 1, 2003, 304 (2) 634-642; DOI: https://doi.org/10.1124/jpet.102.042622

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Research ArticleINFLAMMATION AND IMMUNOPHARMACOLOGY

Effect of β2-Adrenergic Receptor Stimulation on Interleukin-18-Induced Intercellular Adhesion Molecule-1 Expression and Cytokine Production

Hideo Kohka Takahashi, Toshihiko Morichika, Hiromi Iwagaki, Tadashi Yoshino, Ryuji Tamura, Shinnya Saito, Shuji Mori, Tadaatsu Akagi, Noriaki Tanaka and Masahiro Nishibori
Journal of Pharmacology and Experimental Therapeutics February 1, 2003, 304 (2) 634-642; DOI: https://doi.org/10.1124/jpet.102.042622
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