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慢性应激引起的肠道微生物群变化会损害氟西汀的疗效。

Changes in Gut Microbiota by Chronic Stress Impair the Efficacy of Fluoxetine.

机构信息

Institut Pasteur, Perception and Memory Unit, 75015 Paris, France; Centre National de la Recherche Scientifique (CNRS), Unité Mixte de Recherche 3571, 75015 Paris, France.

Institut Pasteur, Microenvironment and Immunity Unit, 75724 Paris, France; Institut National de la Santé et de la Recherche Médicale (INSERM) U1224, 75724 Paris, France.

出版信息

Cell Rep. 2020 Mar 17;30(11):3682-3690.e6. doi: 10.1016/j.celrep.2020.02.099.

Abstract

Major depressive disorders (MDDs) constitute a leading cause of disability worldwide and current pharmacological treatments are partially effective. The gut microbiota (GM) has recently emerged as a target of therapeutic interest for MDDs. In this study, we transfer GM from mice that sustained unpredictable chronic mild stress (UCMS) to healthy recipient mice. The fecal transfer induces despair-like behavior, decreases neurogenesis in the hippocampus (HpC), and impairs the antidepressant and neurogenic effects of a standard selective serotonin (5-HT) reuptake inhibitor, fluoxetine (FLX). These effects are paralleled by deficits in 5-HT bioavailability, biosynthesis, and reuptake in the HpC. Treatment with 5-hydroxytryptophan restores the levels of 5-HT and its precursors in the HpC, improves HpC neurogenesis, and alleviates despair-like symptoms. Our results reveal that stress-induced changes in GM are involved in the pathogenesis of depressive disorders and minimize FLX efficacy via alterations in the serotonergic pathway of Trp metabolism.

摘要

重度抑郁症(MDDs)是全球致残的主要原因,目前的药物治疗部分有效。肠道微生物群(GM)最近成为 MDDs 的治疗靶点。在这项研究中,我们将经历不可预测的慢性轻度应激(UCMS)的小鼠的 GM 转移到健康的受体小鼠中。粪便转移会导致类似绝望的行为,减少海马(HpC)中的神经发生,并损害标准选择性 5-羟色胺(5-HT)再摄取抑制剂氟西汀(FLX)的抗抑郁和神经发生作用。这些影响与 HpC 中 5-HT 生物利用度、生物合成和再摄取的缺陷相平行。5-羟色氨酸治疗可恢复 HpC 中 5-HT 及其前体的水平,改善 HpC 神经发生,并缓解类似绝望的症状。我们的结果表明,GM 中应激诱导的变化参与了抑郁障碍的发病机制,并通过色氨酸代谢的 5-HT 途径的改变最小化了 FLX 的疗效。

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