Schedlowski M, Hosch W, Oberbeck R, Benschop R J, Jacobs R, Raab H R, Schmidt R E
Department of Medicine and Dermatology, Hannover Medical School, Germany.
J Immunol. 1996 Jan 1;156(1):93-9.
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.
儿茶酚胺水平升高已被证明可诱导淋巴细胞尤其是自然杀伤(NK)细胞迁移发生变化。为分析儿茶酚胺诱导NK细胞迁移的机制,对正常健康男性受试者和脾切除个体静脉输注肾上腺素(0.10微克/千克/分钟)、去甲肾上腺素(0.15微克/千克/分钟)或氯化钠,持续20分钟。两种儿茶酚胺给药后淋巴细胞亚群(CD3⁺、CD4⁺、CD8⁺)短暂增加,输注肾上腺素后NK细胞数量(CD16⁺或CD56⁺)增加最为明显(高达600%)。NK细胞数量和功能的这些变化既未伴随NK细胞上黏附分子(CD11a、CD11b、CD31、CD43、CD44、CD62L)表达的改变,也未伴随可溶性黏附分子(sVCAM-1、sICAM-1、sE-选择素)血浆浓度的变化。在脾切除受试者中观察到淋巴细胞亚群有类似增加,提示淋巴细胞从脾脏以外的其他来源募集。此外,儿茶酚胺诱导的淋巴细胞亚群增加可被非选择性β-肾上腺素能受体拮抗剂普萘洛尔预处理抑制,但不能被β1-选择性拮抗剂比索洛尔抑制。这些数据表明,肾上腺素和去甲肾上腺素通过不依赖脾脏的β2-肾上腺素能受体机制调节人类NK细胞的迁移能力。