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.
- Adrenergic receptor
- Intercellular adhesion molecule-1 (ICAM-1)
- Tumour necrosis factor (TNF)-α
ASJC Scopus subject areas
- Cell Biology
- Biochemistry, medical