Connor T J, Kelly J P, McGee M, Leonard B E
Department of Pharmacology, National University of Ireland, Galway.
Life Sci. 2000 Aug 18;67(13):1601-12. doi: 10.1016/s0024-3205(00)00743-8.
In this study we examined the effects of methylenedioxymethamphetamine (MDMA) administration on responsiveness to an in vivo immune challenge with lipopolysaccharide (LPS; 100 microg/kg; i.p.). LPS produced an increase in circulating IL-1beta and TNF-alpha in control animals. MDMA (20 mg/kg; i.p.) significantly impaired LPS-induced IL-1beta and TNF-alpha secretion. The suppressive effect of MDMA on IL-1beta secretion was transient and returned to control levels within 3 hours of administration. In contrast, the MDMA-induced suppression of TNF-alpha secretion was evident for up to 12 hours following administration. In a second study we examined the effect of co-administration of MDMA (5, 10 and 20 mg/kg; i.p.) on LPS-induced IL-1beta and TNF-alpha secretion, and demonstrated that all three doses potently suppressed LPS-induced TNF-alpha secretion, but only MDMA 10 and 20 mg/kg suppressed LPS-induced IL-1beta secretion. In addition, serum MDMA concentrations displayed a dose-dependent increase, with the concentrations achieved following administration of 5 and 10 mg/kg being in the range reported in human MDMA abusers. In order to examine the possibility that the suppressive effect of MDMA on IL-1beta and TNF-alpha could be due to a direct effect of the drug on immune cells, the effect of in vitro exposure to MDMA on IL-1beta and TNF-alpha production in LPS-stimulated diluted whole blood was evaluated. However IL-1beta or TNF-alpha production were not altered by in vitro exposure to MDMA. In conclusion, these data demonstrate that acute MDMA administration impairs IL-1beta and TNF-alpha secretion following an in vivo LPS challenge, and that TNF-alpha is more sensitive to the suppressive effects of MDMA than is IL-1beta. However the suppressive effect of MDMA on IL-1beta and TNF-alpha could not be attributed to a direct effect on immune cells. The relevance of these findings to MDMA-induced immunomodulation is discussed.
在本研究中,我们检测了给予亚甲基二氧甲基苯丙胺(MDMA)对体内脂多糖(LPS;100微克/千克;腹腔注射)免疫刺激反应性的影响。LPS使对照动物循环中的白细胞介素-1β(IL-1β)和肿瘤坏死因子-α(TNF-α)增加。MDMA(20毫克/千克;腹腔注射)显著损害LPS诱导的IL-1β和TNF-α分泌。MDMA对IL-1β分泌的抑制作用是短暂的,给药后3小时内恢复到对照水平。相比之下,MDMA诱导的TNF-α分泌抑制在给药后长达12小时都很明显。在第二项研究中,我们检测了联合给予MDMA(5、10和20毫克/千克;腹腔注射)对LPS诱导的IL-1β和TNF-α分泌的影响,结果表明所有三个剂量均能有效抑制LPS诱导的TNF-α分泌,但只有10和20毫克/千克的MDMA抑制LPS诱导的IL-1β分泌。此外,血清MDMA浓度呈剂量依赖性增加,5和10毫克/千克给药后达到的浓度在人类MDMA滥用者报告的范围内。为了检测MDMA对IL-1β和TNF-α的抑制作用可能是由于药物对免疫细胞的直接作用这一可能性,评估了体外暴露于MDMA对LPS刺激的稀释全血中IL-1β和TNF-α产生的影响。然而,体外暴露于MDMA并未改变IL-1β或TNF-α的产生。总之,这些数据表明急性给予MDMA会损害体内LPS刺激后的IL-1β和TNF-α分泌,并且TNF-α比IL-1β对MDMA的抑制作用更敏感。然而,MDMA对IL-1β和TNF-α的抑制作用不能归因于对免疫细胞的直接作用。讨论了这些发现与MDMA诱导的免疫调节的相关性。