M. Schedlowski et al., CATECHOLAMINES MODULATE HUMAN NK CELL CIRCULATION AND FUNCTION VIA SPLEEN-INDEPENDENT BETA(2)-ADRENERGIC MECHANISMS, The Journal of immunology, 156(1), 1996, pp. 93-99
Increases in catecholamines have been shown to induce changes in migra
tion of lymphocytes, in particular NK cells. To analyze the mechanisms
of catecholamine-induced NK cell trafficking, normal healthy male hum
an subjects and splenectomized individuals were infused with either ad
renaline (0.10 mu g/kg/min), noradrenaline (0.15 mu g/kg/min), or NaCl
i.v. for 20 min. Lymphocyte subsets (CD3(+), CD4(+), CD8(+)) transien
tly increased after administration of both catecholamines, with most p
ronounced 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 adhe
sion 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 s
ubsets were observed in splenectomized subjects, suggesting lymphocyte
recruitment from other sources than the spleen. Furthermore, catechol
amine-induced increases in lymphocyte subsets could be inhibited by pr
etreatment with the nonselective beta-adrenoceptor antagonist proprano
lol, but not by the beta(1)-selective antagonist bisoprolol. These dat
a demonstrate that adrenaline and noradrenaline modulate the migratory
capacity of human NK cells via spleen-independent beta(2)-adrenocepto
r mechanisms.