Depression Promotes the Onset of Irritable Bowel Syndrome through Unique Dysbiosis in Rats.

Abstract:

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.

journal_name

Gut Liver

journal_title

Gut and liver

authors

Takajo T,Tomita K,Tsuchihashi H,Enomoto S,Tanichi M,Toda H,Okada Y,Furuhashi H,Sugihara N,Wada A,Horiuchi K,Inaba K,Hanawa Y,Shibuya N,Shirakabe K,Higashiyama M,Kurihara C,Watanabe C,Komoto S,Nagao S,Kimura K,Mi

doi

10.5009/gnl18296

subject

Has Abstract

pub_date

2019-05-15 00:00:00

pages

325-332

issue

3

eissn

1976-2283

issn

2005-1212

pii

gnl18296

journal_volume

13

pub_type

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