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Gut microbiota, kynurenine pathway and mental disorders - Review.
The intestine and the gut-associated limphoid tissue constitute the largest immunity organ of the human body. Among several possible tryptophan metabolism routes, the kynurenine pathway can be influenced by the gut microbiota. Disturbances of gut biodiversity may cause increased gut permeability and cause systemic inflammation, also related to central nervous system. Proinflammatory cytokines induce kynurenine pathway enzymes resulting in formation of neuroactive metabolites, which are being associated with several psychiatric disorders. The kynurenine pathway may also be influenced by certain bacteria species directly. The aim of this review is to highlight the current knowledge on the interaction of gut microbiota and the central nervous system with the kynurenine pathway taken into special account. Up to date study results on specific psychiatric disorders such as schizophrenia, bipolar disorder, Alzheimer's disease, autism spectrum disorders, depression and alcoholism are presented. Available evidence suggests that toxicity of kynurenine metabolites may be reduced by adjunction of probiotics which can affect proinflammatory cytokines. Due to their potential for modulation of the kynurenine pathway, gut microbiota pose an interesting target for future therapies.
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Therapeutic Implications of the Microbial Hypothesis of Mental Illness.
There is increasingly compelling evidence that microorganisms may play an etiological role in the emergence of mental illness in a subset of the population. Historically, most work has focused on the neurotrophic herpesviruses, herpes simplex virus type 1 (HSV-1), cytomegalovirus (CMV), and Epstein-Barr virus (EBV) as well as the protozoan, Toxoplasma gondii. In this chapter, we provide an umbrella review of this literature and additionally highlight prospective studies that allow more mechanistic conclusions to be drawn. Next, we focus on clinical trials of anti-microbial medications for the treatment of psychiatric disorders. We critically evaluate six trials that tested the impact of anti-herpes medications on inflammatory outcomes in the context of a medical disorder, nine clinical trials utilizing anti-herpetic medications for the treatment of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) or schizophrenia, and four clinical trials utilizing anti-parasitic medications for the treatment of schizophrenia. We then turn our attention to evidence for a gut dysbiosis and altered microbiome in psychiatric disorders, and the potential therapeutic effects of probiotics, including an analysis of more than 10 randomized controlled trials of probiotics in the context of schizophrenia, bipolar disorder (BD), and major depressive disorder (MDD).
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Oleoylethanolamide-producing Lactobacillus paracasei F19 improves metabolic and behavioral disorders by restoring intestinal permeability and microbiota-gut-brain axis in high-fat diet-induced obese male mice.
Metabolic and mood disorders elicited by chronic exposure of high-fat diet (HFD) are often associated with intestinal dysbiosis and persistent low-grade inflammation in the small intestine. This leads to remodeling of the epithelial barrier with disruption of the neuroepithelial circuits that control energy homeostasis by the gut-brain axis. Therefore, therapies that restoreintestinal microbial niche and barrier function are promising candidates to counter peripheral metabolic challenges that affect behaviors controlled by the brain. The endogenous oleoylethanolamine (OEA) was found to shape the intestinal microbiota profile towards a "lean-like phenotype", ameliorating pathological profiles of metabolic diseases. Further, OEA displays beneficial effects in several cognitive paradigms and preserves the epithelial barrier integrity, acting as an intestinal "gate-keeper". Here, we developed an "intestinal OEA factory" for the in-situ and controlled release of OEA by using a probiotic-based delivery system. We engineered the Lactobacillus paracasei F19 (LP) to express the human N-acylphosphatidylethanolamine-preferring phospholipase D (NAPEpld) gene and to produce OEA in response to dietary ultra-low oleate supply. We treated 12-week HFD male mice with oleate-probiotic formulations and assessed their impact on metabolic and behavioral dysfunctions, and microbiota-gut-brain signaling after 8 weeks of treatment. NAPE-expressing LP (pNAPE-LP) led to significant reduced weight loss and improved metabolic dysfunction in HFD-treated mice. Further, a parallel improvement in depressive- and anxiety-like phenotypes was associated with the duodenal barrier function retrieval, the restoration of the Firmicutes/Bacteroidetes ratio, and an increase in beneficial bacteria, such as Lactobacillus, Prevotella, and Parabacteroides. The HFD-driven changes both in the enteric and central nervous system were prevented by pNAPE-LP/oleate treatment. Collectively, our data suggest that these effects were mediated by the oleate-dependent release of OEA by pNAPE-LP since no significant effects were observed in HFD mice treated with the native probiotic alone (pLP). This oleate-regulated delivery system of OEA is a safe and efficient probiotic-based strategy for the treatment of metabolic syndrome and related behavioral disorders.
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The involvement of the gut microbiota in postoperative cognitive dysfunction based on integrated metagenomic and metabolomics analysis.
As the population ages and medical technology advances, anesthesia procedures for elderly patients are becoming more common, leading to an increased prevalence of postoperative cognitive dysfunction. However, the etiology and correlation between the gut microbiota and cognitive dysfunction are poorly understood, and research in this area is limited. In this study, mice with postoperative cognitive dysfunction were found to have reduced levels of fatty acid production and anti-inflammatory flora in the gut, and Bacteroides was associated with increased depression, leading to cognitive dysfunction and depression. Furthermore, more specific microbial species were identified in the disease model, suggesting that modulation of host metabolism through gut microbes may be a potential avenue for preventing postoperative cognitive dysfunction.
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Unveiling the therapeutic potential of the gut microbiota-brain axis: Novel insights and clinical applications in neurological disorders.
Over the last several years, the gut microbiota-brain axis has been the focus of medical study, demonstrating the bidirectional nature of gut and brain communication and the resulting influence on neurological and mental health. Trillions of microorganisms, particularly those found in the gastrointestinal tract, contribute the most to the pathophysiology recovery of organs that are critical to human health, such as digestive processes and metabolism, immune responses, and even cognitive function. Dysbiosis (a disturbance in the microbiome balance) has been identified as one of the risk factors for neuropsychiatric illnesses such as depression, anxiety, autism spectrum disorder, Parkinson's disease, and Alzheimer's disease. Therapeutic strategies aimed at the gut microbiota, such as probiotics, dietary modifications, prebiotics, and fecal microbiota transplantation, will eventually offer ways to alleviate symptoms associated with these disorders by restoring microbial balance, modulating the immune response, and influencing the production of major neurotransmitters. Innovative drug carriers, such as microbially-derived nanoparticles and probiotics that target particular parts of the gut or microbial communities, may improve pharmaceutical treatment efficacy and specificity. The resolution of difficulties such as ethical concerns, unexpected repercussions, and peak performance optimization in a clinical setting is critical for the advancement of this subject.
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Gut microbiota composition associated with alterations in cardiorespiratory fitness and psychosocial outcomes among breast cancer survivors.
PURPOSE: In this proof-of-concept pilot study, our purpose was to determine correlations between gut microbiota composition and alterations in cardiorespiratory fitness and psychosocial outcomes among post-primary treatment breast cancer survivors (BCS). METHODS: Composition of the gut microbiota in BCS (n = 12) was assessed at baseline (M0) and at the end of 3 months (M3) using Illumina MiSeq DNA Sequencing of the 16S rRNA gene. Gut microbiota composition was analyzed using the QIIME bioinformatics software and represented through diversity metrics and taxa analyses. Cardiorespiratory fitness, fatigue, anxiety, depression, and sleep dysfunction were assessed at M0 and M3 via the submaximal treadmill test, Fatigue Symptom Inventory, Hospital Anxiety and Depression Scale, and Pittsburgh Sleep Quality Index, respectively. RESULTS: Increased fatigue interference in BCS was associated with increased mean within-sample Shannon diversity (organism richness and evenness) (p = 0.009). Weighted UniFrac analysis (shifts in taxa relative abundance) revealed significant differences in between-sample (beta) diversity for changes in fatigue interference (p = 0.01) and anxiety (p = 0.022), with a trend observed for fatigue intensity and sleep dysfunction (p < 0.1). Unweighted UniFrac analysis (shifts in taxa types) found significant beta diversity differences for cardiorespiratory fitness (p = 0.026). Prior to false discovery correction (FDR), changes in fitness, fatigue, anxiety, and sleep dysfunction were associated with the frequency of certain gut bacteria genera (e.g., Faecalibacterium, Prevotella, Bacteroides) (p < 0.05). CONCLUSIONS: Correlations may exist between alterations in gut microbiota composition and longitudinal changes in cardiorespiratory fitness, fatigue, and anxiety in BCS. Further research examining the role of the microbiota-gut-brain axis in exercise-induced effects on psychosocial outcomes in BCS is warranted.
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Xiao-Yao-San suppresses psychological distress-related colorectal cancer metastasis and enhances antitumor immune responses through regulating gut microbiota-bile acid axis.
BACKGROUND: Psychiatric disorders are recognized as risk factors for tumor progression and metastasis in colorectal cancer (CRC). Xiao-Yao-San (XYS), a traditional Chinese herbal formula with antidepressant properties, has been reported to inhibit CRC growth and modulate gut microbiota. However, its efficacy and underlying mechanisms in preventing metastasis remain unclear. METHODS: The antimetastatic effect of XYS was assessed in a chronic restraint stress (CRS)-induced CRC model. XYS-associated gut microbiota was evaluated using 16S ribosomal RNA (rRNA) sequencing. Peripheral bile acid (BA) profiles were analyzed through targeted metabolomics. Fecal microbiota and commercial bacterial strains were anaerobically cultured to identify bile salt hydrolase (bsh)-expressing bacteria. XYS-mediated antitumor immune responses were determined via flow cytometry, immunohistochemistry, and cytotoxic T lymphocytes (CD8⁺ T cells)-murine colon adenocarcinoma cell line (MC38) co-culture assays. RESULTS: Administration of dried XYS decoction powder reduced liver metastatic nodules and prevented body weight loss in CRS-induced CRC mice, while also alleviating depressive-like behaviors and lowering serum stress hormone levels. High-dose XYS (2 g/kg/day) produced antimetastatic and antidepressant effects comparable to those of sertraline, although these effects were largely abolished in mice treated with antibiotic cocktails. XYS significantly modulated gut microbiota composition and serum BA profiles, particularly by restoring bsh-expressing bacteria in the cecum and increasing the proportion of free BAs. XYS also reshaped the immune landscape within metastatic foci, where enhanced antitumor CD8⁺ T cell responses were strongly associated with the altered BA profile. Among these, hyocholic acid (HCA), a free BA elevated by XYS, suppressed liver metastasis in vivo, alleviated exhaustion and restored effector function of CD8⁺ T cells in metastatic tumor microenvironment (TME), together with dose-dependently enhanced CD8+ T cell cytotoxicity against tumor cells in vitro. CONCLUSION: XYS prevents psychiatric disorder-associated CRC metastasis and strengthens antitumor immune responses by regulating bsh-expressing gut bacteria and their derived BA profiles. These findings thus offer a novel mechanistic rationale for the potential use of XYS in treating CRC patients with comorbid psychiatric disorders.
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Study on gut microbiota and metabolomics in postmenopausal women.
Menopausal syndrome, occurring during the menopausal stage in women, manifests as symptoms stemming from decreased estrogen levels, such as hot flashes, insomnia, mental disorders (anxiety, depression), and osteoporosis. The bulk of studies have indicated alterations in the gut microbiota of those experiencing menopause syndrome compared to healthy women. However, This article focuses on the alterations in gut microbiota in perimenopausal women. Our study utilized 16 s rRNA sequencing to determine the differences in the gut microbiota and metabolites among 44 menopausal syndrome women. The distribution of gut microbiota in postmenopausal women varies based on the level of follicle stimulating hormone, with changes in gut microbiota abundance taking precedence over symptom onset. Fecal metabolites reveal changes in several metabolites, including Amino acid metabolism (Tyrosine, Tryptophan), Lipid metabolism (Alpha linolenic acid metabolism), and other metabolites. Disturbances in lipid metabolism, triggered by hormonal level fluctuations, can contribute to the development of osteoporosis.
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Gut microbiota manipulation as an epilepsy treatment.
Many studies have documented the important role of the gut microbiota (GM) in the regulation of several central nervous system (CNS) processes through the microbiota-gut-brain (MGB) axis. This latter represents the connection between the CNS, the enteric nervous system, the gut and its microbiota through several ascending and descending pathways. The variation of the GM composition is associated with the pathogenesis and/or progression as well as severity of various neuropsychiatric/neurological diseases such as depression, autism spectrum disorder, multiple sclerosis, Parkinson's, and Alzheimer's diseases. Recently, changes in the bacterial composition of the GM have also been linked to epilepsy and seizures, with some studies exploring the potential role of GM in the regulation of neuronal hyperexcitability, seizure occurrence and epileptogenesis. Accordingly, there are potential novel treatments which are currently being investigated such as probiotics, prebiotics and symbiotic that may represent innovative therapeutic approaches. The aim of this review is to explore the effect of gut microbiota manipulation as a therapeutic strategy in epilepsy and the methodological challenges to design (translational) clinical trial investigating the gut microbiota.
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Gut Microbiota is Altered in Patients with Alzheimer's Disease.
Previous studies suggest that gut microbiota is associated with neuropsychiatric disorders, such as Parkinson's disease, amyotrophic lateral sclerosis, and depression. However, whether the composition and diversity of gut microbiota is altered in patients with Alzheimer's disease (AD) remains largely unknown. In the present study, we collected fecal samples from 43 AD patients and 43 age- and gender-matched cognitively normal controls. 16S ribosomal RNA sequencing technique was used to analyze the microbiota composition in feces. The composition of gut microbiota was different between the two groups. Several bacteria taxa in AD patients were different from those in controls at taxonomic levels, such as Bacteroides, Actinobacteria, Ruminococcus, Lachnospiraceae, and Selenomonadales. Our findings suggest that gut microbiota is altered in AD patients and may be involved in the pathogenesis of AD.