Abstract
The mechanism of bipolar disorder is unclear. Growing evidence indicates that gut microbiota plays a pivotal role in mental disorders. This study aimed to find out changes in the gut microbiota in bipolar depression (BD) subjects following treatment with quetiapine and evaluate their correlations with the brain and immune function. Totally 36 subjects with BD and 27 healthy controls (HCs) were recruited. The severity of depression was evaluated with the Montgomery-Asberg depression rating scale (MADRS). At baseline, fecal samples were collected and analyzed by quantitative polymerase chain reaction (qPCR). T lymphocyte subsets were measured to examine immune function. Near-infrared spectroscopy (NIRS) was used to assess brain function. All BD subjects received quetiapine treatment (300 mg/d) for four weeks, following which the fecal microbiota and immune profiles were reexamined. Here, we first put forward the new concept of brain-gut coefficient of balance (B-GCB), which referred to the ratio of [oxygenated hemoglobin]/(Bifidobacteria to Enterobacteriaceae ratio), to analyze the linkage between the gut microbiota and brain function. At baseline, the CD3+ T cell proportion was positively correlated with log10 Enterobacter spp count, whereas the correlativity between the other bacteria and immune profiles were negative. Log10 B-GCB was positively correlated with CD3+ T cell proportion. In subjects with BD, counts of Faecalibacterium prausnitzii, Bacteroides–Prevotella group, Atopobium Cluster, Enterobacter spp, and Clostridium Cluster IV were higher, whereas the log10 (B/E) were lower than HCs (B/E refers to Bifidobacteria to Enterobacteriaceae ratio and represents microbial colonization resistance). After treatment, MADRS scores were reduced, whereas the levels of Eubacterium rectale, Bifidobacteria, and B/E increased. The composition of the gut microbiota and its relationship to brain function were altered in BD subjects. Quetiapine treatment was effective for depression and influenced the composition of gut microbiota in patients. Clinical Trial Registration: http://www.chictr.org.cn/index.aspx, identifier ChiCTR-COC-17011401, URL: http://www.chictr.org.cn/listbycreater.aspx.
Highlights
Bipolar disorder caused a high global disease burden [1] with a lifetime prevalence of 1.0% for bipolar-I disorder, 1.1% for bipolar-II disorder, and 2.4% for subthreshold bipolar disorder
We found that among patients with bipolar depression (BD): [1] counts of Faecalibacterium prausnitzii, Bacteroides-Prevotella group, Atopobium Cluster, Enterobacter spp, and Clostridium Cluster IV were significantly increased relative to healthy controls (HCs), whereas microbial colonization resistance was significantly decreased; [2] after treatment, populations of Bifidobacteria and Eubacterium rectale rebounded, and microbial colonization resistance recovered along with the decline of Montgomery-Asberg depression rating scale (MADRS) score; [3] brain-gut coefficient of balance (B-GCB) was positively correlated with CD3+ T cell proportion; and [4] log10 (Enterobacter spp count) was positively correlated with CD3+ T cell proportion
The expansion of Bacteroides-Prevotella group and Enterobacter spp indicates the dysbiosis of gut microbiota [53]
Summary
Bipolar disorder caused a high global disease burden [1] with a lifetime prevalence of 1.0% for bipolar-I disorder, 1.1% for bipolar-II disorder, and 2.4% for subthreshold bipolar disorder. The pathogenesis of bipolar disorder is unclear. Its diagnosis is based on clinical symptoms. It is frequently misdiagnosed as major depressive disorder [2, 3]. The misdiagnosis results in poor therapeutic outcomes [2]. It makes great sense to study the mechanism of bipolar disorder, search for biomarkers, and find novel therapies
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