Department of Psychology & Neuroscience , University of Colorado Boulder, Boulder, Colorado.
Institute of Cognitive Science , University of Colorado Boulder, Boulder, Colorado.
Alcohol Clin Exp Res. 2018 Mar;42(3):531-539. doi: 10.1111/acer.13592. Epub 2018 Feb 2.
In recent years, human and animal studies have converged to support altered inflammatory signaling as a molecular mechanism underlying the pathophysiology of alcohol use disorders (AUDs). Alcohol binds to receptors on immune cells, triggering signaling pathways that produce pro-inflammatory cytokines. Chronic inflammation is associated with tissue damage, which may contribute to negative effects of AUD. Conversely, cannabis is associated with decreased inflammatory signaling, and animal studies suggest that cannabinoids may impact alcohol-induced inflammation. Thus, the impact of cannabis on inflammation in AUDs in humans warrants examination.
We explored the relationship between self-reported alcohol and cannabis use and circulating levels of the pro-inflammatory cytokines interleukin 6 (IL-6), IL-8, and IL-1β in the blood. Among 66 regular drinkers (mean age = 30.08), we examined circulating cytokines and administered questionnaires assessing alcohol consumption and days of cannabis use over the past 90 days. We examined whether alcohol consumption, cannabis use, and gender were associated with changes in circulating cytokines, and whether there was a significant interaction between alcohol and cannabis use predicting blood levels of circulating cytokines.
A positive association between alcohol and IL-6 emerged. We also observed a negative association between cannabis and IL-1β. Follow-up moderation analyses indicated a cannabis by alcohol interaction predicting circulating IL-6, such that cannabis nonusers showed a stronger relationship between alcohol and IL-6 compared to cannabis users.
These preliminary findings suggest that cannabinoid compounds may serve to mitigate inflammation associated with alcohol use. In addition, the present results provide data to inform future investigations, with the goal of ultimately leveraging knowledge of the role of inflammation in AUDs to develop more effective treatments focused on novel immune targets.
近年来，人类和动物研究的结果都支持改变炎症信号作为酒精使用障碍（AUD）病理生理学的分子机制。酒精与免疫细胞上的受体结合，触发产生促炎细胞因子的信号通路。慢性炎症与组织损伤有关，这可能是 AUD 的负面影响的原因之一。相反，大麻与炎症信号的降低有关，动物研究表明大麻素可能会影响酒精引起的炎症。因此，大麻对人类 AUD 中炎症的影响值得研究。
我们探讨了自我报告的酒精和大麻使用与血液中促炎细胞因子白细胞介素 6（IL-6）、IL-8 和 IL-1β的循环水平之间的关系。在 66 名经常饮酒者（平均年龄 30.08 岁）中，我们检查了循环细胞因子，并通过问卷评估了过去 90 天内的酒精消耗和大麻使用天数。我们检查了酒精消耗、大麻使用和性别是否与循环细胞因子的变化相关，以及酒精和大麻使用之间是否存在显著的相互作用，以预测循环细胞因子的血液水平。
观察到酒精与 IL-6 之间呈正相关。我们还观察到大麻与 IL-1β 之间呈负相关。后续的调节分析表明，大麻与酒精的相互作用可以预测循环 IL-6，即大麻非使用者与酒精和 IL-6 之间的关系比大麻使用者更强。
这些初步发现表明，大麻素化合物可能有助于减轻与酒精使用相关的炎症。此外，目前的结果为未来的研究提供了数据，目标是最终利用炎症在 AUD 中的作用的知识，开发针对新型免疫靶点的更有效的治疗方法。
