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Differential co-expression networks of the gut microbiota are associated with depression and anxiety treatment resistance among psychiatric inpatients.
BACKGROUND: Comorbid anxiety and depression are common and are associated with greater disease burden than either alone. Our recent efforts have identified an association between gut microbiota dysfunction and severity of anxiety and depression. In this follow-up, we applied Differential Co-Expression Analysis (DiffCoEx) to identify potential gut microbiota biomarker(s) candidates of treatment resistance among psychiatric inpatients. METHODS: In a sample of convenience, 100 psychiatric inpatients provided clinical data at admission and discharge; fecal samples were collected early during the hospitalization. Whole genome shotgun sequencing methods were used to process samples. DiffCoEx was used to identify clusters of microbial features significantly different based on treatment resistance status. Once overlapping features were identified, a knowledge-mining tool was used to review the literature using a list of microbial species/pathways and a select number of medical subject headlines (MeSH) terms relevant for depression, anxiety, and brain-gut-axis dysregulation. Network analysis used overlapping features to identify microbial interactions that could impact treatment resistance. RESULTS: DiffCoEx analyzed 10,403 bacterial features: 43/44 microbial features associated with depression treatment resistance overlapped with 43/114 microbial features associated with anxiety treatment resistance. Network analysis resulted in 8 biological interactions between 16 bacterial species. Clostridium perfringens evidenced the highest connection strength (0.95). Erysipelotrichaceae bacterium 6_1_45 has been most widely examined, is associated with inflammation and dysbiosis, but has not been associated with depression or anxiety. CONCLUSION: DiffCoEx potentially identified gut bacteria biomarker candidates of depression and anxiety treatment-resistance. Future efforts in psychiatric microbiology should examine the mechanistic relationship of identified pro-inflammatory species, potentially contributing to a biomarker-based algorithm for treatment resistance.
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Relationship Between Depression and Epigallocatechin Gallate from the Perspective of Gut Microbiota: A Systematic Review.
Depression, a serious mental illness, is characterized by high risk, high incidence, persistence, and tendency to relapse, posing a significant burden on global health. The connection between depression and gut microbiota is an emerging field of study in psychiatry and neuroscience. Understanding the gut-brain axis is pivotal for understanding the pathogenesis and treatment of depression. Gut microbes influence depression-like behaviors by impacting the hypothalamic-pituitary-adrenal axis (HPA), monoamine neurotransmitters, immune responses, cell signaling, and metabolic pathways. Tea, widely used in clinical practice to improve neuropsychiatric disorders, contains Epigallocatechin gallate (EGCG), a major ingredient of green tea, which effectively regulates intestinal flora. This review examined the risks and causes of depression, the complications associated with intestinal flora, their role in the development and treatment of depression, and how EGCG may alleviate depression through interactions with gut microbiota and other mechanisms.
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A reply to the commentary on 'The association between gut-health promoting diet and depression: A mediation analysis'.
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Gut-microbiota-brain axis by bile acids in depression.
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Animal and plant protein intake association with mental health, tryptophan metabolites pathways, and gut microbiota in healthy women: a cross-sectional study.
Mental health is affected by tryptophane (TRP) metabolism regulation. Diet-influenced gut microbiome regulates TRP metabolism. Thus, the present study aimed to explore the relationship between type of dietary protein intake, gut microbiota, TRP metabolites homeostasis, and mental well-being in healthy women. 91 healthy females aged 18-50 were recruited based on the study protocol. Validate and reliable questionnaires assessed dietary intake and mental health. Biochemical tests and gut microbiota composition were analyzed following the manufacturer's instructions for each enzyme-linked immune sorbent assay (ELISA) kit and Real-time quantitative polymerase chain reaction (qPCR) methods respectively. Regression methods were used to estimate the considered associations. The results show that in the fully adjusted model, plant protein consumption was partially inversely associated with depression risk (OR = 0.27; 95% CI: 0.06, 1.09; P = 0.06). Higher dietary animal protein intake was marginally associated with psychological distress (OR = 2.59; 95% CI: 0.91, 7.34; P = 0.07). KYN to serotonin ratio was inversely associated with animal protein consumption (ß = 1.10; 95% CI: -0.13, 2.33; P = 0.07). Firmicutes/Bacteriodetes ratio (β = -1.27 × 103, SE = 5.99 × 102, P = 0.03) was lower in the top tertile of plant protein. A partially negative correlation was found between dietary animal protein and Prevotella abundance (β = -9.20 × 1018, SE = 5.04 × 1018, P = 0.06). Overall, significant inverse associations were found between a diet high in plant protein with mental disorders, KYN levels, and Firmicutes to Bacteroidetes ratio while adhering to higher animal protein could predispose women to psychological stress.
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Investigating Chronic Toxicity, Diet, Patient-Reported Outcomes and the Microbiome in Immunotherapy-Treated Metastatic Melanoma Survivors: A New Frontier.
Background/Objectives: Immune checkpoint blockade (ICB) therapies have significantly improved outcomes in metastatic melanoma. However, immune-related adverse events (irAEs) and persistent chronic toxicities (CTs) among this emerging survivor population likely influence different facets of quality of life. This study characterized CT, patient-reported outcomes (PROs), diet, physical activity and gut microbiome features in a cohort of long-term survivors with a history of ICB-treated metastatic melanoma. Methods: Forty-eight patients with a history of metastatic melanoma who initiated ICB treatment at least 3 years earlier and were not currently on treatment were prospectively enrolled from a melanoma survivorship clinic. Participants completed screening questionnaires for depression, anxiety, diet and physical activity. The gut microbiome was characterized via metagenomic sequencing in a subsample (n = 39). Patients' clinicopathological characteristics and experience of irAEs (during treatment) and CT (persisting >6 months after completion of therapy) were extracted retrospectively from the medical record. Results: In the overall cohort, 60% were experiencing CT, while 16% and 20% reported clinically relevant levels of depression and anxiety symptoms, respectively. We observed significant differences in overall gut microbiome composition between survivors with and without CT (p = 0.02). Consumption of fruit and vegetables was inversely associated with anxiety (ρ = 0.3, p = 0.038). Added sugar consumption was correlated with the severity of experienced symptoms (ρ = 0.4, p = 0.003), with pronounced associations across the spectrum of symptoms, including pain, fatigue and shortness of breath (p < 0.05). Conclusions: These results suggest that CT is experienced by a substantial proportion of ICB-treated metastatic melanoma survivors. Patients experiencing CT also showed distinct microbiome features. However, additional research in prospective settings is needed to confirm these hypotheses.
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Saikosaponin A alleviates depressive-like behavior induced by reserpine in mice by regulating gut microflora and inflammatory responses.
Saikosaponin A (SSA), a key ingredient of Chaihu-Shugan-San, has been shown to possess anti-inflammatory, antioxidant and antidepressant properties. Therefore, the present study aimed to investigate the potential mechanism of action and the effect of SSA on reserpine-induced depressive-like symptoms in mice. Establishing mouse model of depression using intraperitoneal injection of reserpine (RSP). Forced swimming test, tail suspension test and sucrose preference test were used to assess depression-like behavior in mice. The results showed that mice exposed to RSP not only showed weight loss and depressive behavior, but also elevated levels of IL-1β and TNF-α, as well as upregulated levels of reactive oxygen species (ROS) and lipid peroxides in the hippocampus. Detection of changes in the intestinal flora of mice using 16S rRNA, it was observed that the intestinal flora changed following SSA treatment. Not only was there an increase in the overall abundance of the intestinal microbiota, but there was also a significant down-regulation of the Firmicutes and an up-regulation of the Verrucomicrobia at the phylum level. Furthermore, SSA treatment markedly improved depressive-like behavior induced by RSP, alleviated damage to the hippocampus, elevated levels of monoamine neurotransmitters, suppressed inflammatory factors in the hippocampus, reduced hippocampal oxidative stress, and restored gut microbiota disruption in RSP-induced mice. The findings propose that SSA has the potential to alleviate depressive symptoms in mice by enhancing monoamine neurotransmitter levels, suppressing hippocampal inflammation, and modifying gut microbial composition.
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Radiation enteropathy-related depression: A neglectable course of disease by gut bacterial dysbiosis.
Radiation enteropathy (RE) is common in patients treated with radiotherapy for pelvic-abdominal cancers. Accumulating data indicate that gut commensal bacteria determine intestinal radiosensitivity. Radiotherapy can result in gut bacterial dysbiosis. Gut bacterial dysbiosis contributes to the pathogenesis of RE. Mild to moderate depressive symptoms can be observed in patients with RE in clinical settings; however, the rate of these symptoms has not been reported. Studies have demonstrated that gut bacterial dysbiosis induces depression. In the state of comorbidity, RE and depression may be understood as local and abscopal manifestations of gut bacterial disorders. The ability of comorbid depression to worsen inflammatory bowel disease (IBD) has long been demonstrated and is associated with dysfunction of cholinergic neural anti-inflammatory pathways. There is a lack of direct evidence for RE comorbid with depression. It is widely accepted that RE shares similar pathophysiologic mechanisms with IBD. Therefore, we may be able to draw on the findings of the relationship between IBD and depression. This review will explore the relationship between gut bacteria, RE, and depression in light of the available evidence and indicate a method for investigating the mechanisms of RE combined with depression. We will also describe new developments in the treatment of RE with probiotics, prebiotics, and fecal microbial transplantation.
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Gut hormones in microbiota-gut-brain cross-talk.
The homeostasis of the gut-brain axis has been shown to exert several effects on physiological and psychological health. The gut hormones released by enteroendocrine cells scattered throughout the gastrointestinal tract are important signaling molecules within the gut-brain axis. The interaction between gut microbiota and gut hormones has been greatly appreciated in gut-brain cross-talk. The microbiota plays an essential role in modulating many gut-brain axis-related diseases, ranging from gastrointestinal disorders to psychiatric diseases. Similarly, gut hormones also play pleiotropic and important roles in maintaining health, and are key signals involved in gut-brain axis. More importantly, gut microbiota can affect the release and functions of gut hormones. This review highlights the role of gut microbiota in the gut-brain axis and focuses on how microbiota-related gut hormones modulate various physiological functions. Future studies could target the microbiota-hormones-gut brain axis to develop novel therapeutics for different psychiatric and gastrointestinal disorders, such as obesity, anxiety, and depression.
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Gut microbiota-SCFAs-brain axis associated with the antidepressant activity of berberine in CUMS rats.
BACKGROUND: The anti-depressant effect of berberine (BBR) has been widely reported. However, the underlying mechanism remains unclear. The microbiota-gut-brain (MGB) axis plays a key role in the pathogenesis of depression. Therefore, we aimed to explore the anti-depressant mechanisms of BBR involving the association of the gut microbiota, neurotransmitters, BDNF, and SCFAs in chronic unpredictable mild stress (CUMS)-induced depressive rats. METHODS: The antidepressant effects of BBR were detected by open-field test, 1 % sucrose preference test and body weight test in CUMS-induced depressive rats. 16S rDNA sequencing was performed to identify the change of gut microbiota. The concentrations of fecal SCFAs were analyzed by GC-MS targeted metabolomics. At the same time, neurotransmitters and BDNF expression were measured by enzyme linked immunosorbent assay (ELISA). RESULTS: BBR improved depression-like behaviors in CUMS rats by increasing the expression of serotonin (5-HT), norepinephrine (NE), dopamine (DA), and BDNF in the hippocampus. BBR regulates Firmicutes, Bacteroidetes, and Lachnospiraceae in depressive rats, resulting in the alteration of the synthesis and metabolism of SCFAs, including acetic, propanoic, and isovaleric acids. LIMITATIONS: Direct evidence that BBR improves depressive behaviors via gut microbiota-SCFAs-brain axis is lacking, and only male rats were investigated in the present study. CONCLUSION: The anti-depressant mechanism of BBR is related to the regulation of the MGB axis via modulating the gut microbiota-SCFAs-monoamine neurotransmitters/BDNF.