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微生物群的枯竭增加了芬太尼的自我管理,并通过短链脂肪酸改变了状蛋白质组

Rebecca S Hofford^1,2,3, Katherine R Meckel^3,4, Elizabeth J Wiser¹

¹Department of Translational Neuroscience, Wake Forest School of Medicine, Winston-Salem, NC 27101.

|January 2, 2024

概括

在老鼠中操纵肠道微生物组显著影响芬太尼的摄入量和寻找行为. 用短链脂肪酸恢复微生物平衡可以逆转这些影响,突出显示在阿片类药物使用障碍中肠-大脑信号传输.

科学领域:

神经科学是一个神经科学.
微生物学微生物学
药理学药理学是指药理学的学科.

背景情况:

阿片类药物使用障碍 (OUD) 是一个主要的公共卫生问题,由合成阿片类药物 (如芬太尼) 加剧.
肠道微生物组在调节对包括阿片类药物在内的药物反应中的作用是一个新兴的研究领域.

研究的目的:

研究肠道微生物组的变化如何影响芬太尼的摄入量和在临床前模型中寻找行为.
为了确定与芬太尼使用和微生物群状况相关的特定微生物和蛋白质变化.

主要方法:

雄性大鼠通过使用广谱抗生素进行了微生物群枯竭.
进行了药物自我给药,16S rRNA测序和核 accumbens 蛋白质组分析.
使用短链脂肪酸补充剂测试了行为影响的可逆性.

主要成果:

微生物群的枯竭增加了芬太尼的摄入量和寻求戒断后的药物.
特定的肠道细菌种群与药物服用水平相关.
改变的微生物组在芬太尼治疗后显著改变了核 accumbens 的突触蛋白质组.
抗生素诱导的行为变化被短链脂肪酸补充逆转.

结论:

肠-大脑信号通路在阿片类药物使用障碍中具有关键作用.
肠道微生物组是减少芬太尼使用和复发的潜在治疗目标.
进一步的翻译性研究是有必要的,以探索基于微生物的干预措施对OUD.

关键词:

芬太尼 (Fentanyl) 是一种药物.微生物组是一个微生物组.蛋白质组学蛋白质组学自主管理的自治.

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