Abstract |
We examined the effects of beta2-adrenergic receptor (beta2-AR) agonists on monocyte-derived cytokines, interleukin (IL)-18 and IL-12 production in lipopolysaccharide (LPS)-stimulated monocytes derived from human peripheral blood mononuclear cells (PBMCs), as in vitro model of sepsis. The study found that beta2-AR agonists inhibited IL-18 and IL-12 production in monocytes, and that AR agonist activity was antagonized by the selective beta2-AR antagonist, butoxamine. The selective beta2-AR agonists salbutamol and terbutaline induced a similar inhibitory pattern of IL-18 and IL-12 production. IL-12 production induced by LPS was inhibited by anti-IL-18 Ab, but IL-18 production by LPS was not inhibited by anti-IL-12 Ab, showing that LPS induced IL-18 production without IL-12 production. Therefore, the stimulation of beta2-AR might be beneficial in the treatment of sepsis through inhibiting LPS-elicited IL-18.
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Authors | Kenji Mizuno, Hideo Kohka Takahashi, Hiromi Iwagaki, Goutaro Katsuno, Huda A S M Kamurul, Satoru Ohtani, Shuji Mori, Tadashi Yoshino, Masahiro Nishibori, Noriaki Tanaka |
Journal | Immunology letters
(Immunol Lett)
Vol. 101
Issue 2
Pg. 168-72
(Nov 15 2005)
ISSN: 0165-2478 [Print] Netherlands |
PMID | 15998544
(Publication Type: Journal Article)
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Chemical References |
- Adrenergic beta-2 Receptor Agonists
- Adrenergic beta-2 Receptor Antagonists
- Antibodies
- Interleukin-18
- Lipopolysaccharides
- Receptors, Adrenergic, beta-2
- Tumor Necrosis Factor-alpha
- Interleukin-12
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Topics |
- Adrenergic beta-2 Receptor Agonists
- Adrenergic beta-2 Receptor Antagonists
- Antibodies
(immunology)
- Cell Proliferation
(drug effects)
- Humans
- Interleukin-12
(biosynthesis, immunology)
- Interleukin-18
(biosynthesis, immunology)
- Lipopolysaccharides
(antagonists & inhibitors, pharmacology)
- Monocytes
(drug effects, metabolism)
- Receptors, Adrenergic, beta-2
(metabolism)
- Tumor Necrosis Factor-alpha
(immunology, metabolism)
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