beta2-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

Index: J. Int. Med. Res. 32(5) , 465-83, (2004)

Full Text: HTML

Abstract

We examined the effects of beta2-adrenergic receptor (beta2-AR) agonists on the expression of co-stimulatory molecules on lipopolysaccharide (LPS)-stimulated human peripheral blood mononuclear cells. The study found that beta2-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 beta2-AR antagonist, butoxamine. The selective beta2-AR agonists salbutamol and terbutaline induced a similar co-stimulatory molecule expression pattern. The LPS-induced production of tumour necrosis factor-alpha 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 beta2-AR stimulation. This study clearly demonstrated that endogenous catecholamines elicited immunosuppressive effects through beta2-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.