IL-6, but not TNF-α, response to alcohol cues and acute consumption associated with neural cue reactivity, craving, and future drinking in binge drinkers.
IL-6, but not TNF-α, response to alcohol cues and acute consumption associated with neural cue reactivity, craving, and future drinking in binge drinkers.
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DOI：
10.1016/j.bbih.2023.100645
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发表时间：
2023-08
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影响因子：
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临床前研究表明，学习免疫系统对酒精线索和消费的反应可能有助于酒精的药效学特性和/或酒精使用障碍（AUD）的发病机制。从机制上讲，这些免疫改变可能与渴望和酒精消费的增加有关，无论是急性的还是随着时间的推移。我们试图在2020年6月至2021年11月期间进行的随机，平衡，交叉神经影像学实验中描述这种关系。33个狂饮者（BD）和31个非狂饮者，社交饮酒者（SD），人口统计学和心理变量相匹配，在两个独立的7 T功能磁共振成像（fMRI）扫描中暴露于酒精线索和水线索。每次扫描后，酒精味觉测试（ATT）的内隐动机急性酒精。在扫描过程中和扫描后重复收集渴求测量值和血液细胞因子水平，以检查酒精提示和酒精消耗对渴求水平、肿瘤坏死因子α（TNF-α）和白细胞介素6（IL-6）水平的影响。实验后一个月的前瞻性测量参与者的“真实的世界”的饮酒行为进行了近似的慢性效应。BD表现出显着更高的峰值渴望和IL-6水平比SD在响应酒精线索和相对于水的线索。腹内侧前额叶皮层（VmPFC）的信号变化，在酒精-水的对比度正相关的酒精线索条件下的渴望和IL-6水平，相对于水的线索条件下的渴望和IL-6水平，在BD。此外，在控制了对水的渴望和IL-6反应后，峰值渴望和IL-6水平分别与ATT饮酒量和下个月BD饮酒量独立相关。然而，在控制水提示条件反应后，酒精提示条件下TNF-α的释放与两组的渴求、神经激活、IL-6水平、立即和未来的饮酒量无关。总而言之，BD在酒精线索条件下比SD表现出更大的渴望和IL-6释放，这两者都与前额叶线索反应，立即饮酒和随后30天的未来饮酒有关。酒精相关的免疫变化和对饮酒行为的渴望效应可能是相互独立的，或者可能是BD免疫变化影响饮酒动机的共同途径的指示。临床试验NCT 04412824。我们使用了7 T功能磁共振成像，重复血液采样，和生态瞬时评估。渴望和IL-6与前额叶线索反应和未来的饮酒量有关。酗酒者的神经和免疫变化可能会影响饮酒的动机。TNF- α与酗酒行为或酒精提示反应无关。
Preclinical studies suggest learned immune system responses to alcohol cues and consumption may contribute to alcohol's pharmacodynamic properties and/or Alcohol Use Disorder (AUD) pathogenesis. Mechanistically, these immune alterations may be associated with increased craving and alcohol consumption, both acutely and over time. We sought to characterize this relationship in a randomized, counter-balanced, crossover neuroimaging experiment which took place between June 2020–November 2021. Thirty-three binge drinkers (BD) and 31 non-binge, social drinkers (SD), matched for demographic and psychological variables, were exposed to alcohol cues and water cues in two separate 7 T functional magnetic resonance imaging (fMRI) scans. Each scan was followed by the Alcohol Taste Test (ATT) of implicit motivation for acute alcohol. Craving measures and blood cytokine levels were collected repeatedly during and after scanning to examine the effects of alcohol cues and alcohol consumption on craving levels, Tumor necrosis factor alpha (TNF-α), and Interleukin 6 (IL-6) levels. A post-experiment one-month prospective measurement of participants’ “real world” drinking behavior was performed to approximate chronic effects. BD demonstrated significantly higher peak craving and IL-6 levels than SD in response to alcohol cues and relative to water cues. Ventromedial Prefrontal Cortex (VmPFC) signal change in the alcohol-water contrast positively related to alcohol cue condition craving and IL-6 levels, relative to water cue condition craving and IL-6 levels, in BD only. Additionally, peak craving and IL-6 levels were each independently related to ATT alcohol consumption and the number of drinks consumed in the next month for BD, again after controlling for craving and IL-6 repones to water cues. However, TNF-α release in the alcohol cue condition was not related to craving, neural activation, IL-6 levels, immediate and future alcohol consumption in either group after controlling for water cue condition responses. In sum, BD show greater craving and IL-6 release in the alcohol cue condition than SD, both of which were associated with prefrontal cue reactivity, immediate alcohol consumption, and future alcohol consumption over the subsequent 30 days. Alcohol associated immune changes and craving effects on drinking behavior may be independent of one another or may be indicative of a common pathway by which immune changes in BD could influence motivation to consume alcohol. Clinical Trials NCT04412824. We used 7 T fMRI, repeated blood sampling, and ecological momentary assessment. Craving and IL-6 were associated with prefrontal cue reactivity and future alcohol consumption. Neural and immune changes in binge drinkers may influence motivation to consume alcohol. TNF- α was not related to binge drinking behavior or alcohol cue reactivity.
影响因子：
4
作者：
Gruol DL;Hernandez RV;Roberts A
通讯作者：
Roberts A