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Gut unclassified Ruminococcaceae reweights cortical functional gradients and small-world topology with links to mood and diet.
The microbiota-gut-brain axis is a key conduit linking metabolism, mood, and cognition; however, its position within the continuous functional hierarchy of the cortex and the underlying mechanisms are unclear. In this study, a cross-modal brain-gut dataset from 88 healthy male participants was utilized. By integrating functional magnetic resonance imaging (fMRI) gradient analysis, microbiome sequencing, and dietary behavioral information, this study systematically evaluated the relationships between the abundance of unclassified Ruminococcaceae (Ruminococcaceae_unc), cerebral functional hierarchy, network topology, and emotional symptoms. The results demonstrated that increased abundance of this bacterial group was associated with a functional shift in the brain from unimodal to transmodal hubs, accompanied by a drift of the small-world network toward randomization. Functional gradient values were significantly negatively correlated with depression and anxiety scores and were tightly coupled with latent components in the dietary behavioral dimension, including education, physical activity, and nutrient intake. Transcriptomic analysis further revealed that the GPCR-Rho/integrin-vesicular trafficking pathway may serve as the key molecular mechanism. In conclusion, this study proposes a multiscale coupling framework encompassing the gut microbiota, functional gradients, and emotional health, thereby providing a theoretical basis for the development of microbiota-targeted intervention strategies for modulating transmodal emotions and cognition.
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Lactiplantibacillus plantarum fermentation enhances the antidepressant effects of Hemerocallis citrina Baroni in chronic restraint stress mice.
ETHNOPHARMACOLOGICAL RELEVANCE: Hemerocallis citrina Baroni (H. citrina), referred to as 'Forgetting Sadness Grass,' is a traditional Chinese medicine (TCM) known for its antidepressant effects. Fermentation is an ancient processing method for TCM. Whether fermentation affects the antidepressant effect of H. citrina is unknown. AIM: In this study, we aim to evaluate the effect of fermented and unfermented H. citrina on chronic restraint stress-induced depression and the underlying mechanism. MATERIALS AND METHODS: H. citrina was co-fermented with Lactiplantibacillus plantarum strains LZU-J-TSL-6 and LZU-J-LZ1-1 to produce fermented H. citrina (FH). Both H. citrina and FH were evaluated for effects on depression and anxiety in chronic restraint stress (CRS) mice. RESULTS: Fermentation increased flavonoids and phenols while reducing terpenoids. Both H. citrina and FH exhibited antidepressant effects, with FH showing superior efficacy in alleviating depressive symptoms. Specifically, FH effectively alleviated weight loss, behavioral abnormalities, and hippocampal pathological damage caused by CRS, while significantly reducing serum levels of cortisol and inflammatory factors, and increasing hippocampal serotonin (5-HT) level. Moreover, FH can restore CRS-induced gut microbiota dysbiosis by promoting the colonization of beneficial microbes, such as Lactobacillus, and inhibiting the growth of harmful microbes, like Bacteroides_H. Importantly, we discovered that the antidepressant effects of FH are closely associated with substances such as L-theanine and myo-inositol, as well as with the metabolic pathways of alanine, aspartic acid, and glutamic acid. CONCLUSION: Our findings suggest that fermentation alters the composition of active ingredients in H. citrina and enhance its role in depression. It highlights the potential therapeutic application of FH in treating depression.
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Synergistic Antidepressant-like Effects of Biotics and n-3 Polyunsaturated Fatty Acids on Dopaminergic Pathway through the Brain-Gut Axis in Rats Exposed to Chronic Mild Stress.
Probiotics, postbiotics, and n-3 polyunsaturated fatty acids (PUFA) have antidepressant-like effects. However, the underlying mechanisms of the dopaminergic pathway are unclear. The present study investigated the hypothesis that probiotics and postbiotics combined with n-3 PUFA synergistically improve depression by modulating the dopaminergic pathway through the brain-gut axis. Rats were randomly divided into seven groups: non-chronic mild stress (CMS) with n-6 PUFA, and CMS with n-6 PUFA, n-3 PUFA, probiotics, postbiotics, probiotics combined with n-3 PUFA, and postbiotics combined with n-3 PUFA. Probiotics, postbiotics, and n-3 PUFA improved depressive behaviors, decreased blood concentrations of interferon-γ, and interleukin-1β, and increased the brain and gut concentrations of short chain fatty acids and dopamine. Moreover, probiotics, postbiotics, and n-3 PUFA increased the brain and gut expression of glucocorticoid receptor and tyrosine hydroxylase; brain expression of l-type amino acid transporter 1 and dopamine receptor (DR) D1; and gut expression of DRD2. The expression of phosphorylated protein kinase A/protein kinase A and phosphorylated cAMP response element-binding protein/cAMP response element-binding protein increased in the brain, however, decreased in the gut by the supplementation of probiotics, postbiotics, and n-3 PUFA. There was synergistic effect of probiotics and postbiotics combined with n-3 PUFA on the depressive behaviors and dopaminergic pathway in blood, brain, and gut. Moreover, no significant difference in the dopaminergic pathways between the probiotics and postbiotics was observed. In conclusion, probiotics and postbiotics, combined with n-3 PUFA have synergistic antidepressant-like effects on the dopaminergic pathway through the brain-gut axis in rats exposed to CMS.
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Acupuncture improves depression-like behaviors in rats through gut microbiota and TLR4/MyD88/NF-κB pathway modulation.
BACKGROUND: Acupuncture (AP) is used for depression, but mechanisms remain unclear. We asked whether acupuncture attenuates chronic unpredictable mild stress (CUMS)-induced depressive-like behaviors in rats and, specifically, whether its efficacy is linked to remodeling gut microbiota and inhibiting TLR4/MyD88/NF-κB signaling along the gut-brain axis with concomitant rebalancing of hypothalamic-pituitary-adrenal (HPA) activity. METHODS: Male Sprague-Dawley rats underwent CUMS with or without acupuncture. Sucrose preference test (SPT) and forced swim test (FST) assessed behavior. Colonic injury was scored after H&E staining; microbiota were profiled by 16S rDNA sequencing. TLR4/MyD88/NF-κB expression in hypothalamus and colon was measured by Western blot/Real-time PCR; Iba1 + microglia were quantified by immunofluorescence. Serum cytokines and HPA hormones were assayed by ELISA. RESULTS: Acupuncture increased sucrose preference (89.61 ± 2.551 % vs. 73.82 ± 5.711 %, P < 0.05) and reduced FST immobility (20.52 ± 3.784 s vs. 46.13 ± 7.391 s, P < 0.01) versus untreated CUMS. It lowered colonic injury (P < 0.05) and partly restored the Firmicutes/Bacteroidetes ratio. TLR4/MyD88/NF-κB signaling was suppressed in the hypothalamus and colon (TLR4 protein -37 %, P < 0.05), with fewer Iba1 + microglia (27.3 ± 3.2 % vs. 45.6 ± 4.8 %, P < 0.01). Serum IL-6, IL-1β, and TNF-α decreased, and HPA-axis activity normalized. CONCLUSIONS: Acupuncture alleviates CUMS-induced depressive-like behaviors. The benefits are associated with gut microbiota remodeling, inhibition of TLR4/MyD88/NF-κB signaling, and stabilization of HPA-axis function, supporting an immune-microbiota-neuroendocrine mechanism.
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Faecal Short Chain Fatty Acids Profile is Changed in Polish Depressive Women.
Short chain fatty acids (SCFAs) being produced during fermentation of non-digestible polysaccharides are regulatory compounds with the potential to influence inflammatory, as well as emotional state and cognition through the gut⁻brain axis. We analyzed the association between stool concentration of SCFAs (acetic acid (C 2:0), propionic acid (C 3:0), isobutyric acid (C 4:0 i), butyric acid (C 4:0 n), isovaleric acid (C 5:0 i) valeric acid (C 5:0 n), isocaproic acid (C 6:0 i), caproic acid, and (C 6:0 n) heptanoic acid (C 7:0)) and depressive symptoms among women and looked for the potential confounders of microbiota byproduct synthesis. We enrolled 116 women aged 52.0 ± 4.7 years and recognized depression in 47 (40.52%). To analyze the emotional state, Beck's Depression Inventory (BDI) was used. We assessed SCFAs content by means of gas chromatography. Fiber intake was estimated using parts of food frequency questionnaire. The content of acetic acid was significantly lowered compared to non-depressed women (median {IQR}: 29.49 {20.81} vs. 34.99 {19.55}, p = 0.04). A tendency toward decreased level of propionic acid was noticed (median {IQR}: 16.88 {9.73} vs. 21.64 {12.17}, p = 0.07), while the concentration of isocaproic acid was significantly increased in (median {IQR}: 0.89 {1.15} vs. 0.56 {0.95}, p < 0.01) comparison to matched healthy subjects. We found negative correlations between acetate, propionate, and Beck's score (r = -0.2, p = 0.03; r = -0.21, p = 0.02, respectively). Statistically significant correlations between acetate and propionate and BDI somatic score (r = -0.21, p = 0.01; r = -0.17, p = 0.03), as well as correlations regarding isocaproic and both cognitive/affective (r = 0.37, p = 0.0001) and somatic (r = 9.37, p < 0.001) scores were found. Women who declared current usage of lipid-lowering and thyroid drugs in the past, had higher content of C6:0-i (Users; median {IQR}: 1.91 {3.62} vs. non-users; 0.55 {0.67}; p = 0.0048).and lower of C2:0 (Users; median {IQR}: 23.07 {12.80} vs. non users 33.73 {21.44}; p = 0.041), respectively. No correlations regarding SCFAs concentration and fiber intake were found. We concluded that SCFAs may potentially contribute to depression phenotype, however, due to the small size of groups suffering from moderately heavy (n = 5) and severe (n = 7) depression, the conclusion should be treated with caution. Pharmacotherapy of hyperlipidemia and thyroid disease might affect SCFAs synthesis. Studies with more participants are required.
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Exploring the pathogenesis and treatment of PSD from the perspective of gut microbiota.
Post-stroke depression (PSD) is a psychological disease that can occur following a stroke and is associated with serious consequences. Research on the pathogenesis and treatment of PSD is still in the infancy stage. Patients with PSD often exhibit gastrointestinal symptoms; therefore the role of gut microbiota in the pathophysiology and potential treatment effects of PSD has become a hot topic of research. In this review, describe the research on the pathogenesis and therapy of PSD. We also describe how the gut microbiota influences neurotransmitters, the endocrine system, energy metabolism, and the immune system. It was proposed that the gut microbiota is involved in the pathogenesis and treatment of PSD through the regulation of neurotransmitter levels, vagal signaling, hypothalamic-pituitary-adrenal axis activation and inhibition, hormone secretion and release, in addition to immunity and inflammation.
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Vinegar-processed Schisandra Chinensis enhanced therapeutic effects on colitis-induced depression through tryptophan metabolism.
BACKGROUND: Ulcerative colitis (UC) is an inflammatory bowel disease characterized by its incurable nature and undefined etiology, which is often accompanied by a high prevalence of comorbid depression. The gut-brain axis has emerged as a promising treatment target in recent years. PURPOSE: This study aimed to investigate how vinegar-processed Schisandra Chinensis (VSC) enhances therapeutic effects on depressive behavior in chronic UC mice. METHODS: A chronic UC model was induced in mice using dextran sulfate sodium. The therapeutic effects of both raw and vinegar-processed Schisandra Chinensis on UC and associated depressive symptoms were assessed. Colonic mucosal damage was evaluated using hematoxylin and eosin (H&E) and Alcian blue staining. The integrity of the blood-brain barrier (BBB) and synaptic structures was visualized via transmission electron microscopy (TEM). Enzyme-linked immunosorbent assay (ELISA) was employed to quantify inflammatory cytokine levels in the colon, serum, and brain, while western blotting was performed for protein expression analysis. Additionally, metagenomic analysis was conducted to investigate gut microbiota composition. Nissl staining and immunofluorescence were used to assess hippocampal neuronal damage, and behavioral assessments including the morris water maze, open field test, forced swimming test and tail suspension test, were implemented to evaluate depressive states. Serum metabolites were analyzed using UPLC-MS/MS. RESULTS: Both raw and vinegar-processed Schisandra Chinensis significantly upregulated aryl hydrocarbon receptor (AhR), inhibited NF-κB p-p65 activation, and reduced levels of pro-inflammatory cytokine. These treatments also enhanced the expression of tight junction proteins, restored colonic mucosal and BBB integrity, alleviated damage to hippocampal neurons, and improved synaptic structure. Behavioral assessments indicated that VSC was particularly effective in ameliorating depressive-like behaviors in chronic UC mice. In the gut, both treatments reshaped the gut microbial composition, restoring the relative abundance of Duncaniella, Candidatus_Amulumruptor, Alistipes, Parabacteroides, Lachnospiraceae_bacterium, uncultured_Bacteroides_sp., Candidatus_Amulumruptor_caecigallinarius, with VSC showing more pronounced effects. Serum metabolomics revealed an increase in tryptophan levels and a decrease in kynurenine and xanthurenic acid levels with VSC, indicating that tryptophan metabolism shifted from the kynurenine pathway to the 5-HT or indole pathway. However, this phenomenon did not occur with Schisandra Chinensis (SC). CONCLUSION: This study demonstrated that the disruption of tryptophan metabolic balance served as a biological mechanism underlying the occurrence of depressive behaviors induced by UC. The application of SC following vinegar processing enhanced its regulatory effects on gut microbiota and tryptophan metabolism. This findings provided a new insight for the clinical management of gut-brain comorbidities.
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Multi-omics analysis reveals BDE47 induces depression-like behaviors in mice by interfering with the 2-arachidonoyl glycerol-associated microbiota-gut-brain axis.
2,2',4,4'-tetrabromodiphenyl ether (BDE47) is a foodborne environmental risk factor for depression, but the pathogenic mechanism has yet to be fully characterized. In this study, we clarified the effect of BDE47 on depression in mice. The abnormal regulation of the microbiome-gut-brain axis is evidenced closely associated with the development of depression. Using RNA sequencing, metabolomics, and 16s rDNA amplicon sequencing, the role of the microbiome-gut-brain axis in depression was also explored. The results showed that BDE47 exposure increased depression-like behaviors in mice but inhibited the learning memory ability of mice. The RNA sequencing analysis showed that BDE47 exposure disrupted dopamine transmission in the brain of mice. Meanwhile, BDE47 exposure reduced protein levels of tyrosine hydroxylase (TH) and dopamine transporter (DAT), activated astrocytes and microglia cells, and increased protein levels of NLRP3, IL-6, IL-1β, and TNF-α in the brain of mice. The 16 s rDNA sequencing analysis showed that BDE47 exposure disrupted microbiota communities in the intestinal contents of mice, and faecalibaculum was the most increased genus. Moreover, BDE47 exposure increased the levels of IL-6, IL-1β, and TNF-α in the colon and serum of mice but decreased the levels of tight junction protein ZO-1 and Occludin in the colon and brain of mice. In addition, the metabolomic analysis revealed that BDE47 exposure induced metabolic disorders of arachidonic acid and neurotransmitter 2-Arachidonoyl glycerol (2-AG) was one of the most decreased metabolites. Correlation analysis further revealed gut microbial dysbiosis, particularly faecalibaculum, is associated with altered gut metabolites and serum cytokines in response to BDE47 exposure. Our results suggest that BDE47 might induce depression-like behavior in mice through gut microbial dysbiosis. The mechanism might be associated with the inhibited 2-AG signaling and increased inflammatory signaling in the gut-brain axis.
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The role of the gut-brain axis in depression: endocrine, neural, and immune pathways.
The aim of this article is to summarize the pathways connecting the gut and the brain and to highlight their role in the development of depression as well as their potential use as therapeutic targets. A literature search was conducted in PubMed using relevant keywords and their combinations up to the end of March 2020. Previously seen as a disease pertaining solely to the central nervous system, depression is now perceived as a multifactorial condition that extends beyond neurotransmitter depletion. Central to our understanding of the disease is our current knowledge of the communication between the gut and the brain, which is bidirectional and involves neural, endocrine, and immune pathways. This communication is facilitated via stress-mediated activation of the HPA axis, which stimulates the immune system and causes a decrease in microbial diversity, also known as dysbiosis. This change in the intestinal flora leads, in turn, to bacterial production of various substances which stimulate both the enteric nervous system and the vagal afferents and contribute to additional activation of the HPA axis. Concomitantly, these substances are associated with an increase in intestinal permeability, namely, the leaky gut phenomenon. The bidirectional link between the gut and the brain is of great importance for a more inclusive approach to the management of depression. It can thus be deployed for the development of novel therapeutic strategies against depression, offering promising alternatives to limited efficacy antidepressants, while combination therapy also remains a potential treatment option.
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Remodeling of microbiota gut-brain axis using psychobiotics in depression.
Depression is a multifaceted psychiatric disorder mainly orchestrated by dysfunction of neuroendocrine, neurochemical, immune, and metabolic systems. The interconnection of gut microbiota perturbation with the central nervous system disorders has been well documented in recent times. Indeed, alteration of commensal intestinal microflora is noted in several psychiatric disorders such as anxiety and depression, which are presumed to be routed through the enteric nervous system, autonomic nervous system, endocrine, and immune system. This review summarises the new mechanisms underlying the crosstalk between gut microbiota and brain involved in the management of depression. Depression-induced changes in the commensal intestinal microbiota are majorly linked with the disruption of gut integrity, hyperinflammation, and modulation of short-chain fatty acids, neurotransmitters, kynurenine metabolites, endocannabinoids, brain-derived neurotropic factors, hypothalamic-pituitary-adrenal axis, and gut peptides. The restoration of gut microbiota with prebiotics, probiotics, postbiotics, synbiotics, and fermented foods (psychobiotics) has gained a considerable attention for the management of depression. Recent evidence also propose the role of gut microbiota in the process of treatment-resistant depression. Thus, remodeling of the microbiota-gut-brain axis using psychobiotics appears to be a promising therapeutic approach for the reversal of psychiatric disorders, and it is imperative to decipher the underlying mechanisms for gut-brain crosstalk.