β2-Adrenergic receptor stimulation-induced immunosuppressive effects possibly through down-regulation of co-stimulatory molecules, ICAM-1, CD40 and CD14 on monocytes

K. Kuroki, H. K. Takahashi, H. Iwagaki, T. Murakami, M. Kuinose, S. Hamanaka, K. Minami, M. Nishibori, N. Tanaka, K. Tanemoto

Research output: Contribution to journalArticle

23 Citations (Scopus)

Abstract

We examined the effects of β2-adrenergic receptor (β2-AR) agonists on the expression of co-stimulatory molecules on lipopolysaccharide (LPS)-stimulated human peripheral blood mononuclear cells. The study found that β2-AR agonists inhibited the expression of intercellular adhesion molecule-1 (ICAM-1), CD40 and CD14 on monocytes, and that AR agonist activity was antagonized by the selective β2-AR antagonist, butoxamine. The selective β2-AR agonists salbutamol and terbutaline induced a similar co-stimulatory molecule expression pattern. The LPS-induced production of tumour necrosis factor-α. was inhibited by AR agonists, and this was also antagonized by butoxamine, and mimicked by salbutamol and terbutaline. The AR agonists also inhibited T-cell proliferation through β2-AR stimulation. This study clearly demonstrated that endogenous catecholamines elicited immunosuppressive effects through β2-AR stimulation, possibly due to down-regulation of the expression of ICAM-1, CD40 and CD14 on monocytes. These results suggested that the sympathetic nervous system might regulate the T-helper cell balance via the peripheral end-effectors of the stress system.

Original languageEnglish
Pages (from-to)465-483
Number of pages19
JournalJournal of International Medical Research
Volume32
Issue number5
DOIs
Publication statusPublished - 2004

Keywords

  • Adrenergic receptor
  • CD40
  • Intercellular adhesion molecule-1 (ICAM-1)
  • Monocytes
  • Tumour necrosis factor (TNF)-α

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology
  • Biochemistry, medical

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