Huang W, Koller L D
College of Veterinary Medicine, Oregon State University, Corvallis 97331, USA.
Int J Immunopharmacol. 1998 Jan-Mar;20(1-3):39-56. doi: 10.1016/s0192-0561(98)00013-7.
2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is an environmental contaminant that is considered to be a potent immunotoxicant. In the present study, we examined the effect of 25 micrograms/kg TCDD on cytokine production and T lymphocyte phenotype, cell cycling and receptor activity in female Long-Evans rats that had been injected with 50 micrograms of Staphylococcal Enterotoxin B (SEB). In the SEB-injected rats, TCDD increased the serum levels of interleukin-2 (IL-2) but did not affect the serum levels of interleukin-1 (IL-1), interleukin-6 (IL-6) or tumor necrosis factor (TNF). The ability of spleen cells and peritoneal cells to produce cytokines in response to SEB restimulation in vitro was also evaluated. TCDD exposure significantly enhanced IL-2 production by spleen cells from SEB-primed rats after 6 h or 24 h in cultures co-stimulated with SEB in vitro. However, TCDD treatment did not alter the production of IL-6 and TNF in these cultures. Although TCDD did not influence the production of IL-6 and TNF in peritoneal cells from SEB-primed rats with SEB restimultion in vitro, IL-1 production was significantly increased at 2 h. Both the kinetics and extent of SEB-induced IL-2 receptor (IL-2R) and T-cell receptor (TCR) expression on CD4+ cells was unaffected by TCDD. TCDD did not significantly alter the percentage or the total numbers of CD4+ and CD8+ subpopulations at various times after SEB injection. However, flow cytometric analysis showed that TCDD exposure increased the percentage of both CD4+ and CD8+ cells cycling in the S and G2M phase. TCDD, in the absence of SEB priming, did not affect any of the immune parameters tested. Nevertheless, collectively these results showed that TCDD can enhance the production of IL-2 and the percentage of CD4+ and CD8+ cells cycling in SEB-exposed Long-Evans rats. Histopatholgically, there were not observable effects of SEB on lymphoid organs while thymic atrophy and diffuse hepatocellular hypertrophy was observed in the TCDD-treated animals.
2,3,7,8-四氯二苯并-对-二恶英（TCDD）是一种环境污染物，被认为是一种强效免疫毒素。在本研究中，我们检测了25微克/千克TCDD对已注射50微克葡萄球菌肠毒素B（SEB）的雌性Long-Evans大鼠细胞因子产生、T淋巴细胞表型、细胞周期和受体活性的影响。在注射SEB的大鼠中，TCDD增加了白细胞介素-2（IL-2）的血清水平，但不影响白细胞介素-1（IL-1）、白细胞介素-6（IL-6）或肿瘤坏死因子（TNF）的血清水平。还评估了脾细胞和腹腔细胞在体外对SEB再刺激产生细胞因子的能力。在体外与SEB共同刺激的培养物中，TCDD暴露显著增强了SEB致敏大鼠脾细胞在培养6小时或24小时后IL-2的产生。然而，TCDD处理并未改变这些培养物中IL-6和TNF的产生。虽然TCDD在体外对SEB致敏大鼠腹腔细胞在SEB再刺激时IL-6和TNF的产生没有影响，但在2小时时IL-1的产生显著增加。SEB诱导的CD4+细胞上白细胞介素-2受体（IL-2R）和T细胞受体（TCR）表达的动力学和程度均不受TCDD影响。TCDD在SEB注射后不同时间对CD4+和CD8+亚群的百分比或总数没有显著改变。然而，流式细胞术分析表明，TCDD暴露增加了处于S期和G2M期循环的CD4+和CD8+细胞的百分比。在没有SEB致敏的情况下，TCDD对所测试的任何免疫参数均无影响。然而，总体而言，这些结果表明，TCDD可增强SEB暴露的Long-Evans大鼠中IL-2的产生以及处于循环中的CD4+和CD8+细胞的百分比。组织病理学上，SEB对淋巴器官没有可观察到的影响，而在TCDD处理的动物中观察到胸腺萎缩和弥漫性肝细胞肥大。
