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<p>Psychological stress is a major precipitating factor for neuropsychiatric disorders, and the gut-brain axis has emerged as a critical regulator of mood and behavior, but how specific commensal microbes modulate host neurochemistry to confer stress resilience is largely unknown. In this study, we found that chronic restraint stress-induced anxiety- and depression-like behaviors in mice are associated with intestinal microbial imbalance and impaired colonic synthesis of 5-HTP, the direct precursor of serotonin. Concurrently, this leads to reduced serotonin levels both systemically and in the CNS, as well as decreased BDNF in the hippocampus. Notably, supplementation with <i>B. animalis</i> BD1 restored the abundance of beneficial <i>Bifidobacterium</i> and <i>Lactobacillus</i> as well as colonic 5-HTP levels, thereby normalizing serotonin and BDNF expression in the brain, and ultimately ameliorating depression-like behavior in CRS mice. In addition, we found that BD1 influenced synaptic plasticity and the expression level of the microglial surface marker Iba1 in CRS mice. Our findings reveal a key potential possible course of action: <i>B. animalis</i> BD1 rebalances the disturbed gut microbiota, thereby regulating host intestinal tryptophan metabolism, which in turn buffers depression-like behavior in mice under chronic restraint stress.</p><p></p>

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Bifidobacterium animalis subsp. lactis BD1 restores neurotransmitter homeostasis in chronic restraint stress mice via tryptophan metabolic reprogramming

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年8月5日

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  • Meng Tian,
  • Yue Li,
  • Jialin Wang,
  • Ji Wang,
  • Bin Jiang,
  • Yue Leng,
  • Dayong Ren,
  • Binghua Wang

摘要

Psychological stress is a major precipitating factor for neuropsychiatric disorders, and the gut-brain axis has emerged as a critical regulator of mood and behavior, but how specific commensal microbes modulate host neurochemistry to confer stress resilience is largely unknown. In this study, we found that chronic restraint stress-induced anxiety- and depression-like behaviors in mice are associated with intestinal microbial imbalance and impaired colonic synthesis of 5-HTP, the direct precursor of serotonin. Concurrently, this leads to reduced serotonin levels both systemically and in the CNS, as well as decreased BDNF in the hippocampus. Notably, supplementation with B. animalis BD1 restored the abundance of beneficial Bifidobacterium and Lactobacillus as well as colonic 5-HTP levels, thereby normalizing serotonin and BDNF expression in the brain, and ultimately ameliorating depression-like behavior in CRS mice. In addition, we found that BD1 influenced synaptic plasticity and the expression level of the microglial surface marker Iba1 in CRS mice. Our findings reveal a key potential possible course of action: B. animalis BD1 rebalances the disturbed gut microbiota, thereby regulating host intestinal tryptophan metabolism, which in turn buffers depression-like behavior in mice under chronic restraint stress.