Kelley Sheila P, Moynihan Jan A, Stevens Suzanne Y, Grota Lee J, Felten David L
Center for Psychoneuroimmunology Research, University of Rochester Medical Center, 300 Crittenden Boulevard, Rochester, New York 14642, USA.
Brain Behav Immun. 2002 Apr;16(2):118-39. doi: 10.1006/brbi.2001.0627.
Numerous studies have shown that alterations in sympathetic nervous system (SNS) function produced by beta-adrenergic receptor blockade or chemical sympathectomy can produce changes in T and B lymphocyte function and both innate and acquired immune responses. However, fewer studies have investigated changes in immune response following SNS alterations in animal models of disease. We tested whether blocking SNS activity using 6-OHDA or the beta-receptor antagonist nadolol alters the typical pattern in production of T helper 1 (Th1) and Th2 cytokines seen in cultures of spleen cells from C57BL/6 mice infected with murine AIDS (MAIDS). We found that neither method of sympathetic blockade affected cytokine response to MAIDS. We also found that the norepinephrine concentration and content of the spleen were reduced dramatically by the MAIDS infection itself at 3 and 6 weeks after LP-BM5 inoculation. This finding has not been previously reported in mice with MAIDS and suggests that the viral infection itself produces a functional sympathectomy in the spleen, a target of that infection.
大量研究表明，β-肾上腺素能受体阻断或化学性交感神经切除术所导致的交感神经系统（SNS）功能改变，可引起T和B淋巴细胞功能以及先天性和获得性免疫反应的变化。然而，较少有研究在疾病动物模型中探究SNS改变后的免疫反应变化。我们测试了使用6-羟基多巴胺（6-OHDA）或β受体拮抗剂纳多洛尔阻断SNS活性，是否会改变感染鼠类获得性免疫缺陷综合征（MAIDS）的C57BL/6小鼠脾细胞培养物中辅助性T细胞1（Th1）和辅助性T细胞2（Th2）细胞因子产生的典型模式。我们发现，两种交感神经阻断方法均未影响对MAIDS的细胞因子反应。我们还发现，接种LP-BM5后3周和6周，MAIDS感染本身会使脾脏中的去甲肾上腺素浓度和含量显著降低。这一发现此前在患有MAIDS的小鼠中尚未见报道，表明病毒感染本身会在脾脏（该感染的一个靶器官）产生功能性交感神经切除术。
