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Multi-omics analyses of serum metabolome, gut microbiome and brain function reveal dysregulated microbiota-gut-brain axis in bipolar depression.
The intricate processes of microbiota-gut-brain communication in modulating human cognition and emotion, especially in the context of mood disorders, have remained elusive. Here we performed faecal metagenomic, serum metabolomics and neuroimaging studies on a cohort of 109 unmedicated patients with depressed bipolar disorder (BD) patients and 40 healthy controls (HCs) to characterise the microbial-gut-brain axis in BD. Across over 12,000 measured metabolic features, we observed a large discrepancy (73.54%) in the serum metabolome between BD patients and HCs, spotting differentially abundant microbial-derived neuroactive metabolites including multiple B-vitamins, kynurenic acid, gamma-aminobutyric acid and short-chain fatty acids. These metabolites could be linked to the abundance of gut microbiota presented with corresponding biosynthetic potentials, including Akkermansia muciniphila, Citrobacter spp. (Citrobacter freundii and Citrobacter werkmanii), Phascolarctobacterium spp., Yersinia spp. (Yersinia frederiksenii and Yersinia aleksiciae), Enterobacter spp. (Enterobacter cloacae and Enterobacter kobei) and Flavobacterium spp. Based on functional neuroimaging, BD-related neuroactive microbes and metabolites were discovered as potential markers associated with BD-typical features of functional connectivity of brain networks, hinting at aberrant cognitive function, emotion regulation, and interoception. Our study combines gut microbiota and neuroactive metabolites with brain functional connectivity, thereby revealing potential signalling pathways from the microbiota to the gut and the brain, which may have a role in the pathophysiology of BD.
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The endocannabinoidome as a substrate for noneuphoric phytocannabinoid action and gut microbiome dysfunction in neuropsychiatric disorders .
The endocannabinoid (eCB) system encompasses the eCBs anandamide and 2-arachidonoylglycerol, their anabolic/catabolic enzymes, and the cannabinoid CB1 and CB2 receptors. Its expansion to include several eCB-like lipid mediators, their metabolic enzymes, and their molecular targets, forms the endocannabinoidome (eCBome). This complex signaling system is deeply involved in the onset, progress, and symptoms of major neuropsychiatric disorders and provides a substrate for future therapeutic drugs against these diseases. Such drugs may include not only THC, the major psychotropic component of cannabis, but also other, noneuphoric plant cannabinoids. These compounds, unlike THC, possess a wide therapeutic window, possibly due to their capability of hitting several eCBome and non-eCBome receptors. This is particularly true for cannabidiol, which is one of the most studied cannabinoids and shows promise for the treatment of a wide range of mental and mood disorders. The eCBome plays a role also in the microbiota-gut-brain axis, which is emerging as an important actor in the control of affective and cognitive functions and in their pathological alterations. .
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Microbiome and metabolic disruption in acute vs. severe and enduring anorexia nervosa.
Anorexia nervosa (AN) is associated with profound alterations in gut microbiota and host metabolic profiles. While previous studies have primarily focused on the acute phase of AN, the chronic form, severe and enduring anorexia nervosa (SEAN), remains underexplored in terms of microbiome dynamics. In this study, we characterized gut microbiota composition (via 16S rRNA gene amplicon sequencing), serum and fecal metabolites (via mass spectrometry), and an extensive range of clinical, anthropometric, biochemical, and psychiatric parameters in females with acute AN, SEAN, and in healthy controls. SEAN patients exhibited higher antidepressant usage and greater lifetime stress exposure. Acute AN patients presented with more pronounced eating disorder severity and depressive symptoms. Elevated levels of intestinal fatty acid-binding protein in SEAN patients suggest mucosal damage. Microbiota analysis revealed reduced alpha diversity and distinct community composition in both AN groups, with SEAN showing the greatest interindividual variability. Both AN cohorts exhibited significantly lower serum and fecal γ-aminobutyric acid (GABA) levels, which were negatively correlated with taxa such as Christensenellaceae, Ruminococcaceae, and Escherichia-Shigella, i.e., microorganisms potentially associated with GABA degradation or impaired synthesis. Additionally, reductions in short-chain fatty acids suggest impaired microbial fermentation and dysregulation of the gut-brain axis. Collectively, these findings reveal progressive, functionally relevant changes in microbiota-host interactions in SEAN. These alterations likely reflect the persistent disease state and may contribute to its continuation.
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Curcumin Alleviates DSS-Induced Anxiety-Like Behaviors via the Microbial-Brain-Gut Axis.
The anxiety and depression caused by inflammatory bowel diseases (IBD) are known to greatly affect the mental health of patients. The mechanism of psychiatric disorders caused by IBD is not fully understood. Previous research has suggested that the gut microbiome plays a key role in IBD. Curcumin is a yellow polyphenol extracted from the rhizome of the ginger plant, which has been shown to have effects against both depression and anxiety. Research has indicated that curcumin affects the gut microbiome and exerts antianxiety and neuroprotective effects through the microbiota-gut-brain axis (MGB). However, whether curcumin can alleviate the psychiatric disorders caused by IBD and how curcumin affects the MGB axis through the gut microbiota have not been fully understood. Therefore, this study was aimed at determining the metabolic parameters and microbiological environment in the peripheral and central nervous system to determine the effects of curcumin against anxiety induced by dextran sulfate sodium salt (DSS) in mice. To elaborate on the link between the gut microbiota and how curcumin alleviates anxiety-like behaviors, we performed a fecal microbiota transplantation (FMT) experiment. The results suggested that curcumin can effectively relieve anxiety-like behaviors caused by DSS in mice. Further, curcumin treatment can alleviate disturbances in the gut microbiota and systemic disorders of lipid metabolism caused by DSS. Finally, through FMT, we verified that curcumin increased phosphatidylcholine in the prefrontal cortex of the mice and alleviated DSS-induced anxiety-like behaviors by modulating specific gut microbiota. We also revealed that Muribaculaceae may be a key part of the gut microbiota for curcumin to alleviate DSS-induced anxiety-like behaviors through the MGB axis.
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Sex-specific relationships of the infant microbiome and early-childhood behavioral outcomes.
BACKGROUND: A link between the gut microbiome and behavior is hypothesized, but most previous studies are cross-sectional or in animal models. The modifying role of host sex is poorly characterized. We aimed to identify sex-specific prospective associations between the early-life gut microbiome and preschool-age neurobehavior. METHODS: In a prospective cohort, gut microbiome diversity and taxa were estimated with 16S rRNA sequencing at 6 weeks, 1 year, and 2 years. Species and gene pathways were inferred from metagenomic sequencing at 6 weeks and 1 year. When subjects were 3 years old, parents completed the Behavioral Assessment System for Children, second edition (BASC-2). A total of 260 children contributed 523 16S rRNA and 234 metagenomics samples to analysis. Models adjusted for sociodemographic characteristics. RESULTS: Higher diversity at 6 weeks was associated with better internalizing problems among boys, but not girls [βBoys = -1.86 points/SD Shannon diversity; 95% CI (-3.29, -0.42), pBoys = 0.01, βGirls = 0.22 (-1.43, 1.87), pGirls = 0.8, pinteraction = 0.06]. Among other taxa-specific associations, Bifidobacterium at 6 weeks was associated with Adaptive Skills scores in a sex-specific manner. We observed relationships between functional features and BASC-2 scores, including vitamin B6 biosynthesis pathways and better Depression scores. CONCLUSIONS: This study advances our understanding of microbe-host interactions with implications for childhood behavioral health. IMPACT: This is one of the first studies to examine the early-life microbiome and neurobehavior, and the first to examine prospective sex-specific associations. Infant and early-childhood microbiomes relate to neurobehavior including anxiety, depression, hyperactivity, and social behaviors in a time- and sex-specific manner. Our findings suggest future studies should evaluate whether host sex impacts the relationship between the gut microbiome and behavioral health outcomes.
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Lactobacillus from the Altered Schaedler Flora maintain IFNγ homeostasis to promote behavioral stress resilience.
The gut microbiome consists of trillions of bacteria, fungi, and viruses that inhabit the digestive tract. These communities are sensitive to disruption from environmental exposures ranging from diet changes to illness. Disruption of the community of lactic acid producing bacteria, Lactobaccillacea, has been well documented in mood disorders and stress exposure. In fact, oral supplement with many Lactobacillus species can ameliorate these effects, preventing depression- and anxiety-like behavior. Here, we utilize a gnotobiotic mouse colonized with the Altered Schaedler Flora to remove the two native species of Lactobaccillacea: L. intestinalis and L. murinus. Using this microbial community, we found that the Lactobacillus species themselves, and not the disrupted microbial communities are protective from environmental stressors. Further, we determine that Lactobaccillacea are maintaining homeostatic IFNγ levels which are mediating these behavioral and circuit level responses. By utilizing the Altered Schaedler Flora, we have gained new insight into how probiotics influence behavior and provide novel methods to study potential therapies to treat mood disorders.
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Gut microbial signatures and differences in bipolar disorder and schizophrenia of emerging adulthood.
INTRODUCTION: Gut microbial disturbance has been established as potential pathogenesis of mental disorders. However, the signatures and differences regarding patients with schizophrenia (SCH) or bipolar disorder (BD) in emerging adulthood as well as their subtypes have been poorly addressed. METHODS: In the present study, stool samples obtained from 63 emerging adult patients with schizophrenia (SCH), 50 with bipolar disorder (BD), and 40 healthy controls (HC) were analyzed by 16 S rRNA gene sequencing; psychiatric symptoms and psychological, social, and professional functioning were also assessed. RESULTS: We found that gut microbiota composition was remarkably changed in the patients with SCH and BD. Moreover, the distinct gut microbiome signatures and their potential function in bipolar depression (BP-D) and SCH with predominantly negative symptoms (SCH-N) as well as bipolar mania (BP-M) and SCH with predominantly positive symptoms (SCH-P) were also observed. Furthermore, we identified diagnostic potential biomarkers that can distinguish BD from HC (38 genera, AUC = 0.961), SCH from HC (32 genera, AUC = 0.962), and BD from Scheme (13 genera, AUC = 0.823). Potential diagnostic biomarkers that can distinguish BD-D from SCH-N (16 genera, AUC = 0.969) and BD-M from SCH-P (31 genera, AUC = 0.938) were also identified. CONCLUSION: This study provides further understanding of abnormal gut microbiome in emerging adulthood patients with SCH and BD and lay the potential foundation for the development of microbe-based clinical diagnosis for BD and SCH.
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Xiaohuafuning tang intervenes liver-depression-and-spleen-deficiency syndrome chronic-atrophic-gastritis by reshaping amino acid metabolism through gut Microbiota.
BACKGROUND: Xiaohua Funing Tang (XHFND) is a decoction formula of traditional Chinese medicine (TCM) and possesses the potential to manage chronic atrophic gastritis (CAG) with liver depression and spleen deficiency (LDSD), but the mechanisms were still unclear. PURPOSE: Our aim is to reveal the overall synergistic mechanisms of XHFND against CAG with LDSD. METHODS: Based on a CAG rat model with LDSD, this study combined metabolomics, gut microbiota, and network pharmacology techniques to demonstrate the XHFND mechanisms with multiple components and targets. RESULTS: Through the integration analysis of gut microbiome and metabolome using metorigin, we found that XHFND regulates arginine metabolism levels in the urea cycle by regulating the gut ecological environment and the host. The XHFND mainly promotes aspartate 1 metabolism by regulating the abundance of odoribacter, bacteroides, phocaeicola, lachnospire, and intestinimonas, intervened in the imbalance of arginine metabolism in CAG rats with LDSD, suppresses the pathogenic Th17 cell differentiation, and inhibits the gastric mucosa damage in rats. Through Cytoscape analysis of network pharmacology and metabolomics integration, we found that XHFND might regulate host phospholipid metabolism through PTEN and PIK3CA to inhibit the PI3K-AKT-TSC axis and then inhibit mTORC1 to control arginine metabolism in the urea cycle and produce polyamines, thereby inhibiting the pathogenic Th17 cell differentiation and preventing rat gastric mucosa damage. Intervention in arginine metabolism in the urea cycle is the primary pathway in which XHFND exerts its therapeutic effects. XHFND may mainly control the pathogenic Th17 cell differentiation in the gastric mucosa of model rats through the pathway. CONCLUSION: This study indicated that XHFND might intervene in treating CAG with LDSD from multiple levels and perspectives to suppress the pathogenic Th17 cell differentiation, which aligns with the characteristics of TCM treatment. This study presents experimental evidence for the clinical use of XHFND and promotes the development of drugs for the therapy of CAG with LDSD.
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Altered gut bacterial-fungal interkingdom networks in patients with current depressive episode.
INTRODUCTION: Bacterial dysbiosis has been described in patients with current depressive episode (CDE); however, the fungal composition in the gut has not been investigated in these patients. METHODS: Here, we characterized the fungal gut mycobiota in patients with CDE. We systematically characterized the microbiota and mycobiota in fecal samples obtained from 24 patients with CDE and 16 healthy controls (HC) using 16S rRNA gene- and ITS1-based DNA sequencing, respectively. RESULTS: In patients with CDE, bacterial dysbiosis was characterized by an altered composition and reduced correlation network density, and the gut mycobiota was characterized by a relative reduction in alpha diversity and altered composition. Most notably, the CDE group had higher levels of Candida and lower level of Penicillium than the HC group. Compared with the HC group, the gut microbiota in patients with CDE displayed a significant disruption in the bacteria-fungi correlation network suggestive of altered interkingdom interactions. Furthermore, a gut microbial index based on the combination of eight genera (four bacterial and four fungal CDE-associated genera) distinguished CDE patients from controls with an area under the curve of approximately 0.84, suggesting that the gut microbiome signature is a promising tool for disease classification. CONCLUSIONS: Our findings suggest that both bacteria and fungi contribute to gut dysbiosis in patients with CDE. Future studies involving larger cohorts and metagenomic or metabolomic analyses may clarify the structure and potential roles and functions of the gut mycobiome and its impact on the development of CDE.
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Limosilactobacillus fermentum 2L Ameliorates Chronic Stress-Induced Neuroinflammation through Gut-Brain Axis Modulation in Mice.
Chronic stress contributes to neuroinflammation and psychiatric disorders through gut-brain axis dysregulation. This study investigated the therapeutic potential of Limosilactobacillus fermentum 2L in ameliorating stress-induced neuroinflammation using an unpredictable chronic mild stress (UCMS) model. Five L. fermentum strains were screened for probiotic properties, with strain 2L selected based on superior acid and bile tolerance, cellular adhesion, and antioxidant activity. C57BL/6J mice underwent 7-week UCMS with concurrent 10-weeks of 2L treatment (109 CFU/day). Behavioral assessments, histological analysis, qRT-PCR, Western blotting, and gut microbiome analysis were performed. Strain 2L demonstrated superior gastrointestinal survival and anti-inflammatory properties in LPS-challenged HT-29 cells. In UCMS mice, 2L treatment significantly ameliorated anxiety- and depression-like behaviors, preserved hippocampal neuronal morphology, and normalized hypothalamic-pituitary-adrenal (HPA) axis dysfunction by reducing elevated corticosterone levels (155.9 ± 17.2 to 121.3 ± 3.1 ng/ml, p < 0.001). Molecular analysis revealed restored hippocampal BDNF expression, normalized serotonin receptors (HTR1A, 5HT7R), and attenuated stress-activated MAPK pathways (ERK1/2, JNK1/2). Treatment restored intestinal barrier integrity through tight junction protein upregulation and reduced pro-inflammatory cytokine expression. Microbiome analysis showed successful Limosilactobacillus colonization with restoration of beneficial bacteria (Faecalibaculum, Akkermansia) and normalization of stress-elevated Prevotella. L. fermentum 2L provides multifaceted neuroprotection through gut-brain axis modulation, involving microbiota restoration, intestinal barrier strengthening, HPA axis normalization, and enhanced neuroplasticity. These findings support the therapeutic potential of targeted probiotic interventions for stress-related neuropsychiatric disorders.