You can manage bookmarks using lists, please log in to your user account for this.
Media type:
E-Article
Title:
Catecholamines modulate human NK cell circulation and function via spleen-independent beta 2-adrenergic mechanisms
Contributor:
Schedlowski, M;
Hosch, W;
Oberbeck, R;
Benschop, R J;
Jacobs, R;
Raab, H R;
Schmidt, R E
Published:
The American Association of Immunologists, 1996
Published in:
The Journal of Immunology, 156 (1996) 1, Seite 93-99
Language:
English
DOI:
10.4049/jimmunol.156.1.93
ISSN:
0022-1767;
1550-6606
Origination:
Footnote:
Description:
Abstract Increases in catecholamines have been shown to induce changes in migration of lymphocytes, in particular NK cells. To analyze the mechanisms of catecholamine-induced NK cell trafficking, normal healthy male human subjects and splenectomized individuals were infused with either adrenaline (0.10 microgram/kg/min), noradrenaline (0.15 microgram/kg/min), or NaCl i.v. for 20 min. Lymphocyte subsets (CD3+, CD4+, CD8+) transiently increased after administration of both catecholamines, with most pronounced increases (up to 600%) in NK cell numbers (CD16+ or CD56+) after infusion of adrenaline. These changes in NK cell numbers and function were accompanied neither by alterations in expression of adhesion molecules (CD11a), CD11b, CD31, CD43, CD44, CD62L) on NK cells nor by changes in plasma concentrations of soluble (s) adhesion molecules (sVCAM-1, sICAM-1, sE-selectin). Comparable increases in lymphocyte subsets were observed in splenectomized subjects, suggesting lymphocyte recruitment from other sources than the spleen. Furthermore, catecholamine-induced increases in lymphocyte subsets could be inhibited by pretreatment with the nonselective beta-adrenoceptor antagonist propranolol, but not by the beta1-selective antagonist bisoprolol. These data demonstrate that adrenaline and noradrenaline modulate the migratory capacity of human NK cells via spleen-independent beta 2-adrenoceptor mechanism.