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A cross-sectional study observing the association of psychosocial stress and dietary intake with gut microbiota genera and alpha diversity among a young adult cohort of black and white women in Birmingham, Alabama.
BACKGROUND: The relationships between psychosocial stress and diet with gut microbiota composition and diversity deserve ongoing investigation. The primary aim of this study was to examine the associations of psychosocial stress measures and dietary variables with gut microbiota genera abundance and alpha diversity among young adult, black and white females. The secondary aim was to explore mediators of psychosocial stress and gut microbiota diversity and abundance. METHODS: Data on 60 females who self-identified as African American (AA; n = 29) or European American (EA; n = 31) aged 21-45 years were included. Cortisol was measured in hair and saliva, and 16S analysis of stool samples were conducted. Discrimination experiences (recent and lifetime), perceived stress, and depression were evaluated based on validated instruments. Spearman correlations were performed to evaluate the influence of psychosocial stressors, cortisol measures, and dietary variables on gut microbiota genus abundance and alpha diversity measured by amplicon sequence variant(ASV) count. Mediation analyses assessed the mediating role of select dietary variables and cortisol measures on the associations between psychosocial stress, Alistipes and Blautia abundance, and ASV count. RESULTS: AA females were found to have significantly lower ASV count and Blautia abundance. Results for the spearman correlations assessing the influence of psychosocial stress and dietary variables on gut microbiota abundance and ASV count were varied. Finally, diet nor cortisol was found to partially or fully mediate the associations between subjective stress measures, ASV count, and Alistipes and Blautia abundance. CONCLUSION: In this cross-sectional study, AA females had lower alpha diversity and Blautia abundance compared to EA females. Some psychosocial stressors and dietary variables were found to be correlated with ASV count and few gut microbiota genera. Larger scale studies are needed to explore the relationships among psychosocial stress, diet and the gut microbiome.
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Are neuromodulation interventions associated with changes in the gut microbiota? A systematic review.
The microbiota-gut-brain axis (MGBA) refers to the bidirectional communication between the brain and the gut microbiota and recent studies have linked the MGBA to health and disease. Research has so far investigated this axis mainly from microbiota to brain but less is known about the other direction. One approach to examine the MGBA from brain to microbiota is through understanding if and how neuromodulation might impact microbiota. Neuromodulation encompasses a wide range of stimulation techniques and is used to treat neurological, psychiatric and metabolic disorders, like Parkinson's Disease, depression and obesity. Here, we performed a systematic review to investigate whether neuromodulation is associated with subsequent changes in the gut microbiota. Searches in PsycINFO and MEDLINE were performed up to March 2022. Included studies needed to be clinical or preclinical studies comparing the effects of deep brain stimulation, electroconvulsive therapy, repetitive transcranial magnetic stimulation, transcranial direct current stimulation or vagal nerve stimulation on the gut microbiota before and after treatment or between active and control groups. Seven studies were identified. Neuromodulation was associated with changes in relative bacterial abundances, but not with (changes in) α-diversity or β-diversity. Summarizing, currently reported findings suggest that neuromodulation interventions are associated with moderate changes in the gut microbiome. However, findings remain inconclusive due to the limited number and varying quality of included studies, as well as the large heterogeneity between studies. More research is required to more conclusively establish whether, and if so, via which mechanism(s) of action neuromodulation interventions might influence the gut microbiota.
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Anxiety Disorders and Gut Dysbiosis in Primary Sjögren's Syndrome-Mediated Dry Eye Patients.
PURPOSE: Primary Sjögren's syndrome (pSS), a disease that is associated with a high prevalence of psychological disorders, has become increasingly important. Interactions between the gut microbiota and ocular conditions have been identified in pSS. As mental intervention is frequently needed, this study aims to investigate the relationship between anxiety disorders and the gut microbiome in patients with pSS-mediated dry eye. METHODS: Demographics and self-administered questionnaires were obtained. Faecal samples were evaluated using 16S ribosomal RNA gene sequencing. RESULTS: The Hospital Anxiety and Depression Scale (HADS-A) cut-off point of ≥ 8 points showed a sensitivity and specificity of 76.5% and 80.0%, respectively. In all participants, we found that the prevalence of anxiety disorder was 30.4%. Dry eye discomfort could promote an anxious state, and conversely, anxiety could threaten tear film and increase the risk of pSS activity. There was a certain correlation between anxiety disorder and gut dysbiosis. Prevotella was associated with dry eye severity (p <0.001). Bacteroidetes (p =0.046) and Odoribacter (p =0.001) were correlated with pSS activity. CONCLUSION: There is a bidirectional relationship between anxiety disorder and the gut microbiota in pSS-mediated dry eye. Alterations in certain classes of gut microbiota are associated with pSS activity and dry eye severity. Main gut microbiota alterations that have a facilitating impact on anxiety are emerging in pSS-mediated dry eye. Future studies are needed to explore specific therapeutic targets for improving mental health in pSS-mediated dry eye by microbiota intervention.
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Analysis of gut microbiota and intestinal mucosal neurotransmitter changes and their correlation in adolescent depression mice.
BACKGROUND: Adolescent depression is a major mental health disorder with increasing prevalence and substantial long-term consequences. Although growing evidence suggests that the gut-brain axis is involved in depression, the relationships among gut microbiota, intestinal mucosal neurotransmitters, and adolescent depression remain insufficiently understood. This knowledge gap limits a better understanding of the pathophysiological mechanisms underlying adolescent depression and the identification of potential microbiota-related targets. Therefore, this study aimed to investigate alterations in gut microbiota and intestinal mucosal neurotransmitters, as well as their correlations, in an adolescent mouse model of depression. METHODS: We established an adolescent depression mouse model using chronic unpredictable mild stress (CUMS), and collected data with the Smart video tracking system. We collected intestinal contents and mucosal tissues from mice. We analyzed gut microbial composition using metagenomic sequencing and quantified mucosal neurotransmitters with liquid chromatography-tandem mass spectrometry (LC-MS/MS). We analyzed correlations among gut microbiota, intestinal mucosal neurotransmitters, and behavioral indicators. RESULTS: Mice in the CUMS group exhibited a significantly reduced sucrose preference rate in the sucrose preference test (P < 0.001); a significantly prolonged immobility time in the forced swim test (P < 0.01); and a significantly decreased total movement distance in the open field test (P < 0.01). No significant intergroup difference was observed in the tail suspension test. Regarding the gut microbiome, the CUMS group showed significantly lower Simpson index (P = 0.018) and Pielou's evenness index (P = 0.022). Beta diversity analysis indicated a statistically significant but modest between-group difference in community structure (ANOSIM R = 0.145, P = 0.03); this finding was supported by PERMANOVA (Bray-Curtis; pseudo-F = 1.675, R² = 0.0897, P = 0.033). LEfSe (Linear discriminant analysis Effect Size) analysis suggested 27 candidate taxa with discriminatory signals between groups (nominal P < 0.05; exploratory). Neurotransmitter analysis demonstrated that levels of 5-HIAA (5-hydroxyindoleacetic acid), 5-HT (serotonin), 5-HTP (5-hydroxytryptophan), and Kyn (kynurenine) in the colon were significantly decreased in the CUMS group, whereas levels of PA (phenylethylamine) and NE (norepinephrine) were significantly elevated (P < 0.05). Spearman correlation analysis found that Lactobacillus and Lactobacillus acidophilus correlated positively with sucrose preference and negatively with immobility in the forced swim test. Lactobacillus acidophilus also showed a positive correlation with 5-HT pathway metabolites: 5-HIAA, 5-HT, 5-HTP, and Kyn. CONCLUSION: Adolescent mice exposed to CUMS showed depression-relevant behavioral alterations, shifts in gut microbiota composition, and changes in 5-HT pathway metabolites. Gut microbiota dysbiosis was significantly associated with alterations in 5-HT pathway metabolites. Because this study is correlational, causal relationships require validation in future interventional studies.
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Butyrate ameliorates chronic alcoholic central nervous damage by suppressing microglia-mediated neuroinflammation and modulating the microbiome-gut-brain axis.
BACKGROUND: Alcohol abuse triggers neuroinflammation, leading to neuronal damage and further memory and cognitive impairment. Few satisfactory advances have been made in the management of alcoholic central nervous impairment. Therefore, novel and more practical treatment options are urgently needed. Butyrate, a crucial metabolite of short-chain fatty acids (SCFAs), has been increasingly demonstrated to protect against numerous metabolic diseases. However, the impact of butyrate on chronic alcohol consumption-induced central nervous system (CNS) lesions remains unknown. METHODS: In this study, we assessed the possible effects and underlying mechanisms of butyrate on the attenuation of alcohol-induced CNS injury in mice. Firstly, sixty female C57BL/6 J mice were randomly divided into 4 groups: pair-fed (PF) group (PF/CON), alcohol-fed (AF) group (AF/CON), PF with sodium butyrate (NaB) group (PF/NaB) and AF with NaB group (AF/NaB). Each group was fed a modified Lieber-DeCarli liquid diet with or without alcohol. After six weeks of feeding, the mice were euthanized and the associated indicators were investigated. RESULTS: As indicated by the behavioral tests and brain morphology, dietary NaB administration significantly ameliorated aberrant behaviors, including locomotor hypoactivity, anxiety disorder, depressive behavior, impaired learning, spatial recognition memory, and effectively reduced chronic alcoholic central nervous system damage. To further understand the underlying mechanisms, microglia-mediated inflammation and the associated M1/M2 polarization were measured separately. Firstly, pro-inflammatory TNF-α, IL-1β, and IL-6 in brain and peripheral blood circulation were decreased, but IL-10 were increased in the AF/NaB group compared with the AF/CON group. Consistently, the abnormal proportions of activated and resting microglial cells in the hippocampus and cortex regions after excessive alcohol consumption were significantly reduced with NaB treatment. Moreover, the rectification of microglia polarization (M1/M2) imbalance was found after NaB administration via binding GPR109A, up-regulating the expression of PPAR-γ and down-regulating TLR4/NF-κB activation. In addition to the direct suppression of neuroinflammation, intriguingly, dietary NaB intervention remarkably increased the levels of intestinal tight junction protein occludin and gut morphological barrier, attenuated the levels of serum lipopolysaccharide (LPS) and dysbiosis of gut microbiota, suggesting that NaB supplementation effectively improved the integrity and permeability of gut microecology. Finally, the neurotransmitters including differential Tryptophan (Trp) and Kynurenine (Kyn) were found with dietary NaB administration, which showed significantly altered and closely correlated with the gut microbiota composition, demonstrating the complex interactions in the microbiome-gut-brain axis involved in the efficacy of dietary NaB therapy for alcoholic CNS lesions. CONCLUSION: Dietary microbial metabolite butyrate supplementation ameliorates chronic alcoholic central nervous damage and improves related memory and cognitive functions through suppressing microglia-mediated neuroinflammation by GPR109A/PPAR-γ/TLR4-NF-κB signaling pathway and modulating microbiota-gut-brain axis.
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Bridging the gut and mind: a narrative review of depression in Crohn's disease and emerging gut-brain axis therapies.
Depression is a highly prevalent and clinically significant comorbidity in Crohn's disease (CD), a form of inflammatory bowel disease (IBD), and is associated with increased disease activity, hospitalization, and a reduced quality of life (QoL). While traditionally attributed to the psychosocial burden of chronic illness, emerging evidence indicates that depressive symptoms in CD arise from dysregulation of the gut-brain axis (GBA), a bidirectional network linking immune, microbial, and central nervous system (CNS) processes. Chronic intestinal inflammation, characterized by elevated cytokines such as tumor necrosis factor (TNF-α) and interleukin-6 (IL-6), may influence brain function through vagal signaling, hypothalamic-pituitary-adrenal (HPA) axis activation, and neuroimmune pathways. Concurrently, epithelial barrier dysfunction and microbial dysbiosis promote translocation of bacterial products, further amplifying systemic inflammation and neuroimmune signaling. This review consolidates preclinical and clinical evidence linking immune activation, microbial alterations, and neuroimmune signaling to depression in CD. The review compares emerging therapeutic strategies, such as ketamine enantiomers, vagus nerve stimulation, and microbiota-targeting natural compounds, with established therapies like serotonergic antidepressants, cognitive behavioral therapy, and biologic immunotherapies. Across these modalities, therapeutic effects on mood are heterogeneous and often dissociated from improvements in intestinal inflammation, highlighting the multifunctional nature of GBA dysfunction. Overall, these findings suggest that therapeutic responses in CD-associated depression may depend on the extent to which interventions modulate distinct components of the GBA, including immune, neural, and microbial pathways. These observations emphasize the need for integrative treatment strategies that address the multiple contributors of GBA dysbiosis. Future studies incorporating standardized and emerging psychiatric, immunological, and microbiome outcomes will be critical to identifying mechanisms for specific treatment responses in this population.
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Polyphenol intake and depressive symptoms in young adults: evidence from a population-based longitudinal study.
Due to the high prevalence of depression among young adults, identifying prevention strategies during young adulthood is crucial. Dietary polyphenols have been associated with depression in older cohorts; however, the association remains unclear, particularly in young adults. This study aimed to assess the prospective association between the intake of total polyphenols, polyphenol classes and polyphenol subclasses with depressive symptoms in young adults. Data from 1484 Raine Study Generation 2 participants (52·7 % female; baseline mean age (sd): 20 (0·5)) at the -20, -22, and -27 year follow-ups (n 964, 979 and 1094, respectively), with overlap across follow-ups, were used. Energy-adjusted polyphenol intake was estimated from FFQ data using our expansion of the AUSNUT 2011-13 and Phenol-Explorer to include polyphenol content data and categorised into quartiles. The primary outcome was self-reported depressive symptoms assessed via the twenty-one-item Depression, Anxiety and Stress Scale averaged across the three time points. Linear mixed-effects models were used to assess the association between the polyphenol intake exposures and depressive symptoms. Sociodemographic characteristics and lifestyle- and health-related behaviours were adjusted for. Participants in the highest quartiles for flavonol and hydroxybenzoic acid intake had lower depressive symptoms across time than participants in the lowest quartiles (flavonols (Q4 v. Q1 mean difference: -1.38; 95% CI -2.48, -0.28); hydroxybenzoic acids (Q4 v. Q1: -1.40; 95% CI -2.53, -0.27). We found no evidence of a highest v. lowest association for all other polyphenol categories. Future studies are required to investigate whether increasing polyphenol intake could protect against depression in young adults.
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Chronic Sleep Deprivation Causes Anxiety, Depression and Impaired Gut Barrier in Female Mice-Correlation Analysis from Fecal Microbiome and Metabolome.
BACKGROUND: Chronic sleep deprivation (CSD) plays an important role in mood disorders. However, the changes in the gut microbiota and metabolites associated with CSD-induced anxiety/depression-like behavior in female mice have not been determined. Due to the influence of endogenous hormone levels, females are more susceptible than males to negative emotions caused by sleep deprivation. Here, we aim to investigate how CSD changes the gut microbiota and behavior and uncover the relationship between CSD and gut microbiota and its metabolites in female mice. METHODS: We used a 48-day sleep deprivation (SD) model using the modified multiple platform method (MMPM) to induce anxiety/depression-like behavior in female C57BL/6J mice and verified our results using the open field test, elevated plus maze, novel object recognition test, forced swim test, and tail suspension test. We collected fecal samples of mice for 16S rDNA sequencing and untargeted metabolomic analysis and colons for histopathological observation. We used Spearmen analysis to find the correlations between differential bacterial taxa, fecal metabolites, and behaviors. RESULTS: Our study demonstrates that CSD induced anxiety/depressive-like behaviors in female mice. The results of 16S rDNA sequencing suggested that the relative abundance of the harmful bacteria g_ Rothia, g_ Streptococcus, g_ Pantoea, and g_ Klebsiella were significantly increased, while the beneficial bacteria g_ Rikenella, g_ Eubacterium]-xylanophilum-group, and g_ Eisenbergiella were significantly decreased after SD. Glycerophospholipid metabolism and glutathione metabolism were identified as key pathways in the fecal metabolism related to oxidative stress and inflammatory states of the intestine. Histological observation showed hyperplasia of epithelial cells, a decrease in goblet cells, and glandular atrophy of the colon in SD mice. There were correlations between some of the differential bacterial taxa, fecal metabolites, and behaviors. CONCLUSION: In summary, we found that CSD induced anxiety/depression-like behavior, caused gut microbiota dysbiosis, altered fecal metabolism, and damaged the colon barrier in female mice.
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Dietary resistant starch alleviates Escherichia coli-induced bone loss in meat ducks by promoting short-chain fatty acid production and inhibiting Malt1/NF-κB inflammasome activation.
BACKGROUND: Escherichia coli (E. coli) infection in humans and animals usually comes with gut dysbiosis, which is potential culprit to skeletal health, it is still unclear to whether diet interfered gut microbiome changes can be a protective strategy to bone loss development. Here, the effects of resistant starch from raw potato starch (RPS), a type of prebiotic, on E. coli-induced bone loss and gut microbial composition in meat ducks were evaluated. RESULTS: The results showed that dietary 12% RPS treatment improved bone quality, depressed bone resorption, and attenuated the pro-inflammatory reaction in both ileum and bone marrow. Meanwhile, the 12% RPS diet also increased the abundance of Firmicutes in E. coli-treated birds, along with higher production of short-chain fatty acids (SCFAs) especially propionate and butyrate. Whereas addition of β-acid, an inhibitor of bacterial SCFAs production, to the drinking water of ducks fed 12% RPS diet significantly decreased SCFAs level in cecum content and eliminated RPS-induced tibial mass improvement. Further, treatment with MI-2 to abrogate mucosa-associated lymphoid tissue lymphoma translocation protein 1 (Malt1) activity replicated the protective role of dietary 12% RPS in E. coli-induced bone loss including reduced the inhibition on nuclear factor κB (NF-κB) inflammasome activation, decreased bone resorption, and improved bone quality, which were correlated with comparable and higher regulatory T cells (Treg) frequency in MI-2 and 12% RPS group, respectively. CONCLUSIONS: These findings suggested that the diet with 12% RPS could alleviate E. coli-induced bone loss in meat ducks by changing the gut microbial composition and promoting concomitant SCFAs production, and consequently inhibiting Malt1/NF-κB inflammasome activation and Treg cells expansion.
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The kynurenine pathway storm in epilepsy: mechanisms and therapeutic implications.
The kynurenine pathway (KP) is the main route for tryptophan (TRP) degradation and plays a crucial role in neuroinflammation, oxidative stress and neurotransmission, which holds significant clinical significance. The dysregulation of this pathway is closely related to neurological disorders such as epilepsy, and its metabolic products can promote the occurrence of epileptic seizures and comorbid depression. This review aims to clarify the complex mechanisms of the KP in the occurrence and development of epilepsy and to explore its potential as a therapeutic target for epilepsy and comorbid depression. This is a narrative review and synthesis of the current literature. We reviewed animal experiments and clinical studies, elaborating in detail on how metabolites of the KP and their key enzymes function in the context of epilepsy by regulating neuroinflammation, oxidative stress, glutamatergic signaling, and the gut-brain axis. We also explored the interaction between antiseizure medications (ASMs) and the KP, and evaluated the potential value of targeting key enzymes (such as indoleamine 2,3-dioxygenase, IDO) as a new therapeutic strategy for epilepsy. This review particularly focuses on the promoting effect of KP imbalance on comorbid depression, clarifying how IDO-mediated TRP metabolism changes constitute a common mechanism basis, jointly leading to the occurrence of epilepsy and depression-like behaviors. The occurrence and development of epilepsy are closely related to the imbalance of the KP, specifically manifested as a decrease in kynurenic acid (KYNA) level and an increase in quinolinic acid (QA) level. The IDO-mediated shift of TRP metabolism towards the KP is established as a critical mechanism underlying depression comorbidity in epilepsy. Therapeutic modulation of this pathway, through targeting key enzymes like IDO and restoring the KYNA/QA balance, presents a viable strategy for improving the cerebral microenvironment. This approach holds promise for enhancing seizure control, counteracting drug resistance, and concurrently alleviating comorbid depressive symptoms.