Yoshii H, Tatsumi S, Matsuoka T, Suehiro S, Konishi J, Yanagihara Y, Negoro S, Kishimoto S
Department of Immunology and Allergy, Institute of Bio-Active Science, Nippon Zoki Pharmaceutical Company, Hyogo, Japan.
Int J Immunopharmacol. 1989;11(5):543-50. doi: 10.1016/0192-0561(89)90184-7.
To examine the immunopharmacological actions of an extract isolated from inflamed skin of rabbits inoculated with Vaccinia virus (Neurotropin), its effect on the immune responses in aging BALB/c mice was examined. Neurotropin clearly restored the decreasing T-cell-dependent immune responses such as delayed-type hypersensitivity (DTH) response and plaque-forming cells (PFC) response to sheep red blood cells (SRBC) when administered i.p. from 13 months old (mo) to 16 mo. However, Neurotropin administration from 2 to 5 mo had no effect on the immune responses of young animals. Neurotropin administration from 13 to 16 mo restored not only the T-cell proliferation of spleen cells induced by concanavalin A (Con A) and phytohemagglutinin (PHA), but also the interleukin-2 (IL-2) production by spleen cells activated with Con A. However, Neurotropin did not affect the responsiveness of Con A-activated spleen cells to exogenous recombinant IL-2. An absence of suppressor cells capable of inhibiting the IL-2 production in the spleens was confirmed in the 16 mo mice. Neurotropin administration also restored IL-1 production by peritoneal macrophages stimulated with lipopolysaccharide (LPS). These results suggest that long-term administration of Neurotropin restores the decreasing T-cell-dependent immune responses through the recovery of IL-2 and in part IL-1 production, but not the responsiveness to IL-2 in aging BALB/c mice.
为研究从接种痘苗病毒(神经妥乐平)的兔炎症皮肤中分离出的提取物的免疫药理作用,检测了其对衰老BALB/c小鼠免疫反应的影响。当从13月龄(mo)至16 mo腹腔注射时,神经妥乐平明显恢复了如迟发型超敏反应(DTH)和对绵羊红细胞(SRBC)的空斑形成细胞(PFC)反应等依赖T细胞的免疫反应的下降。然而,2至5 mo时给予神经妥乐平对幼龄动物的免疫反应没有影响。13至16 mo给予神经妥乐平不仅恢复了由刀豆蛋白A(Con A)和植物血凝素(PHA)诱导的脾细胞的T细胞增殖,还恢复了用Con A激活的脾细胞产生白细胞介素-2(IL-2)的能力。然而,神经妥乐平不影响Con A激活的脾细胞对外源重组IL-2的反应性。在16 mo小鼠中证实不存在能够抑制脾脏中IL-2产生的抑制细胞。神经妥乐平给药还恢复了用脂多糖(LPS)刺激的腹腔巨噬细胞产生IL-1的能力。这些结果表明,长期给予神经妥乐平通过恢复IL-2以及部分恢复IL-1的产生,而不是恢复衰老BALB/c小鼠对IL-2的反应性,来恢复下降的依赖T细胞的免疫反应。