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Beta2-adrenergic receptor stimulation inhibits LPS-induced IL-18 and IL-12 production in monocytes.

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.
AuthorsKenji Mizuno, Hideo Kohka Takahashi, Hiromi Iwagaki, Goutaro Katsuno, Huda A S M Kamurul, Satoru Ohtani, Shuji Mori, Tadashi Yoshino, Masahiro Nishibori, Noriaki Tanaka
JournalImmunology letters (Immunol Lett) Vol. 101 Issue 2 Pg. 168-72 (Nov 15 2005) ISSN: 0165-2478 [Print] Netherlands
PMID15998544 (Publication Type: Journal Article)
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
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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