Sopori M L, Kozak W, Savage S M, Geng Y, Soszynski D, Kluger M J, Perryman E K, Snow G E
Division of Pathophysiology, Lovelace Respiratory Research Institute, Albuquerque, NM 87108, USA.
Psychoneuroendocrinology. 1998 Feb;23(2):189-204. doi: 10.1016/s0306-4530(97)00076-0.
Nicotine (NT) treatment impairs T-cell receptor (TCR)-mediated signaling, leading to the arrest of T cells in the G1 phase of the cell cycle and inhibition of the antibody plaque-forming cell (AFC) response to sheep red blood cells (SRBC). This paper summarizes some of the previous findings related to cigarette smoke/NT and the immune response, and presents preliminary evidence suggesting that mice chronically treated with NT (0.5 mg/day/kg body weight) have a depressed inflammatory response in the turpentine-induced abscess model of inflammation. This ability of nicotine to attenuate an inflammatory response may also be the cause of reduced mortality of chronically nicotine-treated mice from acute influenza A pneumonitis. Moreover, in LEW rats, decreased anti-SRBC AFC responses were also observed after intracerebroventricular (i.c.v.) administration of relatively small concentrations of NT (28 micrograms/day/kg body weight) which, when given peripherally, did not affect the AFC response. In vitro the addition of NT to T cells increased protein tyrosine kinase (PTK) activity and intracellular Ca2+ concentration [Ca2+]i. These results support the hypothesis that NT alters immune responses by directly interacting with T cells, as well as indirectly through brain-immune interactions.
尼古丁（NT）处理会损害T细胞受体（TCR）介导的信号传导，导致T细胞在细胞周期的G1期停滞，并抑制对绵羊红细胞（SRBC）的抗体空斑形成细胞（AFC）反应。本文总结了一些先前与香烟烟雾/尼古丁及免疫反应相关的研究结果，并提供了初步证据表明，长期用尼古丁（0.5毫克/天/千克体重）处理的小鼠在松节油诱导的炎症脓肿模型中炎症反应受到抑制。尼古丁减弱炎症反应的这种能力也可能是长期用尼古丁处理的小鼠因急性甲型流感肺炎导致死亡率降低的原因。此外，在LEW大鼠中，脑室内（i.c.v.）给予相对低浓度的尼古丁（28微克/天/千克体重）后，也观察到抗SRBC AFC反应降低，而外周给予该浓度尼古丁时，并不影响AFC反应。在体外，向T细胞中添加尼古丁会增加蛋白酪氨酸激酶（PTK）活性和细胞内Ca2+浓度[Ca2+]i。这些结果支持这样的假说，即尼古丁通过直接与T细胞相互作用以及通过脑-免疫相互作用间接改变免疫反应。
