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首页> 外文期刊>Gut and Liver >Depression Promotes the Onset of Irritable Bowel Syndrome through Unique Dysbiosis in Rats
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Depression Promotes the Onset of Irritable Bowel Syndrome through Unique Dysbiosis in Rats

机译：抑郁症通过大鼠独特的营养不良促进肠易激综合征的发作

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Background/Aims Although studies using conventional animal models have shown that specific stressors cause irritable bowel syndrome (IBS), it is unclear whether depression itself causes IBS. Our aim was to establish a rat model to determine if depression itself promotes the onset of IBS and to elucidate the role of gut microbiota in brain-gut axis pathogenesis during coincident depression and IBS. Methods Rat models of depression were induced using our shuttle box method of learned helplessness. Visceral hypersensitivity was evaluated by colorectal distension (CRD) to diagnose IBS. Gut microbiota compositions were analyzed using high-throughput sequencing. In the subanalysis of rats without depression-like symptoms, rats with posttraumatic stress disorder (PTSD) were also examined. Results The threshold value of CRD in depressed rats was significantly lower than that in control rats. Microbial community analysis of cecal microbiota showed that the relative abundance of Clostridiales incertae sedis , the most prevalent microbe, was significantly lower in depressed rats than in control rats. The distribution pattern of the microbiota clearly differed between depressed rats and control rats. Neither visceral hypersensitivity nor the composition of gut microbiota was altered in rats with PTSD-like phenotypes. Conclusions Our rat model of depression is useful for clarifying the effect of depression on IBS and suggests that depression itself, rather than specific stressors, promotes the onset of IBS. Further, we provided evidence that various psychiatric diseases, viz., depression and PTSD, are associated with unique gut microbiota profiles, which could differentially affect the onset and progression of coincident IBS.
机译：背景/目的尽管使用常规动物模型进行的研究表明，特定的应激源会引起肠易激综合症（IBS），但尚不清楚抑郁症本身是否会导致IBS。我们的目的是建立一个大鼠模型，以确定抑郁症本身是否会促进IBS的发作，并阐明肠道微生物菌群在抑郁症和IBS同时发生时在脑肠轴发病机制中的作用。方法采用学习无助的梭箱法建立抑郁症大鼠模型。通过结肠直肠扩张（CRD）评估内脏超敏反应，以诊断IBS。使用高通量测序分析肠道菌群组成。在没有抑郁样症状的大鼠的亚分析中，还检查了患有创伤后应激障碍（PTSD）的大鼠。结果抑郁大鼠的CRD阈值明显低于对照组。盲肠微生物群的微生物群落分析表明，抑郁症大鼠中最普遍存在的不育梭状芽胞杆菌的相对丰度显着低于对照大鼠。抑郁大鼠和对照大鼠之间的微生物群分布模式明显不同。 PTSD样表型的大鼠内脏超敏反应和肠道菌群的组成都没有改变。结论我们的抑郁症大鼠模型有助于阐明抑郁症对IBS的影响，并表明抑郁症本身而非特定的应激源促进了IBS的发作。此外，我们提供的证据表明，各种精神疾病（即抑郁症和PTSD）与独特的肠道菌群特征有关，这可能会差异性地影响同时发生的IBS的发生和发展。

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