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Microbiota-gut-brain axis and anxiety or depression: A perspective from bibliometric and visual analysis.
BACKGROUND: Anxiety and depression are mental disorders that are prevalent worldwide. Previous studies have shown that it is related to the gut microbiota. The microbiota-gut-brain axis (MGB axis) is a bidirectional signaling pathway that links the gut and central nervous systems. It plays a pivotal role in the development of psychiatric and gastrointestinal disorders, with interactions occurring via the neural, metabolic, immune, and endocrine pathways. This study aimed to reveal the research trends in the MGB axis and anxiety or depression. METHODS: Documents were retrieved from the Web of Science Core Collection with search terms for the microbiota-brain-gut axis and anxiety or depression. CiteSpace and VOSviewer are bibliometric tools used for co-citation analysis, co-occurrence analysis, collaborative network analysis, and keyword citation burst discovery. RESULTS: A total of 1816 published articles were identified, indicating a yearly upward trend. China emerged as the leading contributor, accounting for 497 publications (27.37%). Notably, Nutrients published the most articles, amounting to 77 (4.24%). Regarding authors and institutions, Cryan JF emerged as the frontrunner with remarkable 115 publications, while University College Cork topped the list with 138 articles (7.60%). Keyword analysis highlighted probiotics and inflammation as prominent areas of research, while also revealing the involvement of esteemed scholars in studying the MGB axis and anxiety or depression. CONCLUSION: These findings provide valuable insights into the current study and a future orientation in the field of the MGB axis and anxiety or depression. This information can assist researchers in selecting appropriate journals or collaborators and furthering their studies on the potential mechanisms of anxiety or depression, including their etiology, therapy, prevention, and prognosis.
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Effects of chronic unpredictable mild stress on gut microbiota and fecal amino acid and short-chain fatty acid pathways in mice.
Depression is a serious disease that has a significant impact on social functioning. However, the exact causes of depression are still not fully understood. Therefore, it is necessary to explore new pathways leading to depression. In this study, we used 16 S rDNA to examine changes in gut microbiota and predict related pathways in depression-like mice. Additionally, we employed liquid chromatography-mass spectrometry (LC-MS) to identify changes in amino acids and gas chromatography-mass spectrometry (GC-MS) to identify changes in short-chain fatty acids (SCFAs) in fecal samples. We conducted Pearson/Spearman correlation analysis to investigate the associations between changes in amino acids/SCFAs and behavioral outcomes. The 16 S rDNA sequencing revealed significant alterations in gut microbiota at the phylum and genus levels in mice subjected to chronic unpredictable mild stress (CUMS). The relative abundances of Bacteroidetes, Proteobacteria, Bacteroides, and Alloprevotella were increased, while Firmicutes, Verrucomicrobia, Actinobacteria, Lactobacillus, Akkermansia, Lachnospirillum, and Enterobacter were decreased in the CUMS mice. We used PICRUSt software to annotate the kyoto encyclopedia of genes and genomes (KEGG) pathway function related to depression-like behavior in mice. Our analysis identified sixty functional pathways associated with the gut microbiota of mice exhibiting depression-like behavior. In the amino acid concentration analysis, we observed decreased levels of hydroxyproline and tryptophan, and increased levels of alanine in CUMS mice. In the SCFAs concentration assay, we found decreased levels of butyric acid and valeric acid, and increased levels of acetic acid in CUMS mice. Some of these changes were significantly correlated with depressive-like behaviors. Our study contributes to the understanding of the mechanism of the gut-brain axis in the occurrence and development of depression.
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The Effect of Probiotics on Obesity with Comorbid Depression: A Systematic Review and Meta-Analysis.
Aims/Background Obesity and depression frequently co-occur, and the relationship between them is bidirectional. Being obese or overweight increases the risk of depression, and conversely, depression increases the risk of obesity or overweight. Emerging clinical research has shown that probiotics may be effective in treating obesity and associated depression. Modulating gut microbiota with probiotics may improve obesity-related depression, but current evidence is inconsistent. Methods We systematically searched PubMed, EMBASE, Web of Science, and Cochrane Library for randomized controlled trials examining probiotics for depression in obese adults. Mean difference (MD) in depression scores between probiotic and placebo groups was pooled across studies using random-effects models. Heterogeneity was assessed using I2 to explain heterogeneity in meta-regression analysis. To detect the publication bias of the included studies, a funnel plot, and Begg and Egger tests, were used. Possible heterogeneity moderators were detected by subgroup and sensitivity analyses, Galbraith plot, and graphic display of study heterogeneity (GOSH) analysis. Leave-one-out and Influence analyses were performed to assess sensitivity. Results Five trials (n = 488) were included. Overall, probiotics did not significantly improve depressive symptoms versus placebo (MD = 0.08, 95% confidence interval [CI] = -0.63 to 0.79, p = 0.82). Considerable heterogeneity among studies was observed (I2 = 63%). In subgroup analyses, probiotics significantly reduced depression as measured by the Edinburgh Postnatal Depression Scale (MD = -0.60, 95% CI = -1.17 to -0.03, p = 0.04) with no heterogeneity (I2 = 0%). Probiotics also decreased depressive symptoms after 12 weeks of supplementation (MD = -0.78, 95% CI = -1.58 to -0.01, p = 0.05) versus placebo. No publication bias was found using Begg and Egger tests. The GOSH diagnostics revealed three outliers, among the clusters identified by K-means, DBSCAN (Density-based spatial clustering of applications with noise algorithm), and GMM (Gaussian Mixture Model) analyses. Conclusion Overall, probiotics did not improve depressive symptoms in obesity. However, beneficial effects were observed with the Edinburgh Postnatal Depression Scale and short-term use of probiotic. Additional rigorous randomized controlled trials are warranted to elucidate the therapeutic potential of probiotics for obesity-related depression.
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Antenatal depressive symptoms impair offspring neurodevelopment by inducing maternal gut microbiota dysbiosis during pregnancy.
The effects of maternal antenatal depression (AND) across different stages of pregnancy on offspring neurodevelopment remain poorly understood, and the underlying microbiota-related mechanisms are largely unknown. In a multicenter prospective cohort of 2053 pregnant women, we found that elevated depressive symptoms at any trimester were significantly associated with delayed infant neurodevelopment. Using a nested case‒control design with 16S rRNA sequencing of 504 maternal fecal samples, we identified a consistent reduction of butyrate-producing bacteria and disruption of amino acid metabolism in women with AND symptoms - features that correlated with poorer infant cognitive outcomes. To establish causality, fecal microbiota transplantation (FMT) from women with AND symptoms was administered to germ-free dams, resulting in impaired intestinal barrier integrity, heightened neuroinflammatory signaling, and altered polyunsaturated fatty acid and amino acid metabolism in fetal brains at E18.5, leading to postnatal cognitive deficits in the offspring. Remarkably, maternal butyrate supplementation partially rescued these molecular and neurodevelopmental abnormalities. Together, these findings reveal a mechanistic link between maternal mood, gut microbial ecology, and fetal brain development, and identify the maternal gut microbiota and its metabolites as potential therapeutic targets to prevent the intergenerational effects of antenatal depression.
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Microbiota-metabolome interplay in depression: Metabolic insights and diagnostic potential.
Mounting evidence highlights the interplay between gut microbiota, metabolism, and depression. In this study, we analyze fecal and serum metabolomes in first-episode depression and matched controls (n = 186), with validation in three independent cohorts (n = 223, 85, 52) including drug intervention. Significant disruptions are noted in 53 gut microbial species, 12 microbiota-related metabolic pathways, and 34 metabolites in depressive individuals compared to controls. Sixteen metabolites exhibit reversal after drug administration. Partial Spearman analysis identifies 271 species-metabolite correlations, and mediation analysis unveils 61 metabolite-mediated species-depression correlations. Key features associated with depression, including Bifidobacterium longum, Parasutterella excrementihominis, tyrosine, serotonin, and homovanillic acid, are highlighted. A machine learning model with 34 metabolites achieves area under the receiver operating characteristic (ROC) curve values of 0.82 and 0.80 in discriminating depression from control in test and validation sets. Our findings highlight metabolites as key mediators linking microbiota to depression and as valuable indicators for its identification.
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Lactobacillus reuteri NK33 and Bifidobacterium adolescentis NK98 Alleviate Escherichia coli-Induced depression and Gut Dysbiosis in Mice.
Lactobacillus reuteri NK33 (NK33) and Bifidobacterium adolescentis NK98 (NK98) alleviate immobilization stress-induced depression. To understand the gut microbiota-mediated mechanisms of NK33 and NK98 against depression, we examined their effects on Escherichia coli K1 (K1)-induced depression and gut dysbiosis in mice. NK33, NK98, and their mixtures (1:1, 4:1, and 9:1) mitigated K1-induced depression and colitis. NK33 and NK98 additively or synergistically increased BDNF+/NeuN+ cell population and suppressed NF-κB action in the hippocampus. They alleviated gut dysbiosis by reducing the Proteobacteria population and increasing the Clostridia population. These results suggest that NK33 and NK98 may alleviate depression and colitis by ameliorating gut dysbiosis.
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Ameliorated Effects of Fucoidan on Dextran Sulfate Sodium-Induced Ulcerative Colitis and Accompanying Anxiety and Depressive Behaviors in Aged C57BL/6 Mice.
Fucoidan has shown better effects on the improvement of acute ulcerative colitis (UC). However, the specific mechanisms by which fucoidan improves UC-related behavioral disorders in aged mice, especially its effect on the gut-brain axis, remain to be further explored. C57BL/6 male mice aged 8 months were gavaged with 400 or 100 mg/kg bw day fucoidan for five consecutive weeks, with UC being induced by ad libitum to dextran sulfate sodium (DSS) solution in the fifth week. The results showed that fucoidan ameliorated UC and accompanying anxiety- and depressive-like behaviors with downregulated expressions of (NOD)-like receptor family and pyrin domain-containing 3 (NLRP3), apoptosis-associated speck-like protein (ASC), cysteine aspartate-specific protease-1 (Caspase-1) and interlekin-1β (IL-1β), and elevated mRNA levels of brain-derived neurotrophic factor (Bdnf) and postsynaptic-density protein 95 (Psd-95) in cortex and hippocampus. Furthermore, fucoidan improved the permeability of intestinal barrier and blood-brain barrier and restored the abnormal structure of the gut microbiota with a significantly decreased ratio of Firmicutes to Bacteroidota (F/B) and obviously increased abundance of Akkermansia. As a diet-derived bioactive ingredient, fucoidan might be a better alternative for the prevention of UC and accompanying anxiety- and depressive-like behaviors.
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Microbiota-gut-brain axis: enteroendocrine cells and the enteric nervous system form an interface between the microbiota and the central nervous system.
The microbiota-gut-brain axis transmits bidirectional communication between the gut and the central nervous system and links the emotional and cognitive centers of the brain with peripheral gut functions. This communication occurs along the axis via local, paracrine, and endocrine mechanisms involving a variety of gut-derived peptide/amine produced by enteroendocrine cells. Neural networks, such as the enteric nervous system, and the central nervous system, including the autonomic nervous system, also transmit information through the microbiota-gut-brain axis. Recent advances in research have described the importance of the gut microbiota in influencing normal physiology and contributing to disease. We are only beginning to understand this bidirectional communication system. In this review, we summarize the available data supporting the existence of these interactions, highlighting data related to the contribution of enteroendocrine cells and the enteric nervous system as an interface between the gut microbiota and brain.
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Relative abundance of Akkermansia spp. and other bacterial phylotypes correlates with anxiety- and depressive-like behavior following social defeat in mice.
As discussion of stress and stress-related disorders rapidly extends beyond the brain, gut microbiota have emerged as a promising contributor to individual differences in the risk of illness, disease course, and treatment response. Here, we employed chronic mild social defeat stress and 16S rRNA gene metagenomic sequencing to investigate the role of microbial composition in mediating anxiety- and depressive-like behavior. In socially defeated animals, we found significant reductions in the overall diversity and relative abundances of numerous bacterial genera, including Akkermansia spp., that positively correlated with behavioral metrics of both anxiety and depression. Functional analyses predicted a reduced frequency of signaling molecule pathways, including G-protein-coupled receptors, in defeated animals. Collectively, our data suggest that shifts in microbial composition may play a role in the pathogenesis of anxiety and depression.
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Paeoniflorin Ameliorates Alcohol-Induced Depression via Modulating the Gut-Brain Axis and Inhibiting the NF-κB/NLRP3 Inflammasome Pathway in Mice.
Paeoniflorin (PF), the primary bioactive component of Paeonia plants, exhibits neuroprotective and anti-inflammatory activities. However, its potential role in alcohol-induced depression (AID) through the microbiota-metabolite-brain axis remains unclear. This study aimed to investigate the antidepressant effect of PF and its underlying gut-brain communication mechanisms. A mouse model of chronic alcohol exposure was established and treated with PF. Behavioral tests (SPT, FST, TST, OFT) and histopathological examinations were conducted. Network pharmacology and molecular docking were used to predict targets, followed by experimental validation of microglial activation and the NF-κB/NLRP3 pathway. Multi-omics approaches including 16S rRNA sequencing and untargeted metabolomics were applied to analyze gut microbiota and fecal metabolites. PF significantly alleviated depressive-like behaviors, hippocampal damage, and oxidative stress, while restoring monoamine neurotransmitter levels. It suppressed microglial activation and the NF-κB/NLRP3 inflammasome cascade. Furthermore, PF reshaped gut microbiota composition (reducing Rikenellaceae and Prevotellaceae) and modulated metabolite profiles and upregulated the neuroprotective metabolite niacin, along with other identified metabolites. These findings demonstrate that PF alleviates Alcohol-Induced Depression (AID) by remodeling the microbiota-metabolite-brain axis and inhibiting neuroinflammation. The study highlights PF's therapeutic potential for alcohol-related mood disorders and underscores the gut-brain axis as a critical target for antidepressant therapy.