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Alteration of gut microbiota in migraine patients with irritable bowel syndrome in a Chinese Han population.
OBJECTIVE: Migraine is frequently reported in patients with irritable bowel syndrome (IBS), and emerging evidence suggests that gut microbiota plays a role in migraine and IBS. However, alterations in the gut microbiome in migraine patients with IBS remain unknown. This study aimed to explore the compositions of gut microbiota in migraine patients with IBS in a Chinese Han population. METHODS: Sixteen migraine patients with IBS and thirteen age- and gender-matched IBS patients with similar dietary and lifestyle habits were enrolled in this pilot study. Demographic data, clinical data, eating habits, lifestyle habits, comorbidities, and medications were recorded using a unified case registration form. Questionnaires for the Migraine Disability Assessment (MIDAS), Pittsburgh Sleep Quality Index (PSQI), Hamilton Anxiety Scale (HAMA), and Hamilton Depression Scale (HAMD) were completed. Fecal samples were collected, and microbial DNA was extracted. Gut microbiota 16S ribosomal RNA (16S rRNA) gene sequencing targeting the V4 region was performed using the Illumina HiSeq 2500 high-throughput sequencing platform. The relationships between gut microbiota and clinical characteristics of migraine were analyzed. RESULTS: The structure of gut microbiota differed between migraine patients with IBS and patients with IBS, while the richness and diversity of gut microbiota in migraine patients with IBS showed no significant difference from that of patients with IBS. We found a higher relative abundance of the genus Parabacteroides and a lower relative abundance of the genera Paraprevotella, Lachnospiraceae_UCG-010, Lactococcus, Collinsella, and Comamonas in migraine patients with IBS than in patients with IBS. According to random forest predictive models, the phylum Bacteroidota shows the most important role in migraine patients with IBS. Furthermore, no statistical correlation was found between significantly different taxa at the genus level and migraine clinical data. CONCLUSION: This study identified that altered gut microbiota occurred in Chinese Han migraine patients with IBS, but no correlation was found between gut microbiota and the clinical characteristics of migraine. Further study is needed to better understand the role of gut microbiota in the pathogenesis of migraine in IBS.
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Schaftoside, a functional flavonoid from fenugreek (Trigonella foenum-graecum L.), alleviates depression and cognitive deficits via the microbiome-gut-brain axis in stressed mice.
Depression involves dysregulation of central and peripheral networks, with gut microbiota alterations increasingly implicated in pathogenesis. Trigonella foenum-graecum L. (fenugreek), a functional food and medicinal herb, has been used traditionally for neurological disorders, yet its specific neuroprotective constituents remain poorly characterized. This study evaluated the antidepressant potential of schaftoside, the predominant flavonoid of fenugreek seed flavonoids, and explored its mechanisms involving the microbiome-gut-brain axis in a chronic restraint stress (CRS) mouse model. Male Kunming mice were subjected to CRS and orally administered schaftoside (20, 50, and 125 mg kg-1) or fluoxetine (10 mg kg-1) for 28 days. Behavioral assessments (tail suspension, forced swim, novel object recognition, and Y-maze) demonstrated that schaftoside dose-dependently ameliorated depressive-like behaviors and cognitive impairments. It attenuated hippocampal neuronal damage and neuroinflammation, restoring hippocampal 5-HT, NE, and ACh levels. Intestinal barrier integrity was improved, evidenced by enhanced tight junction proteins (ZO-1, occludin) and mucin (MUC2) expression, alongside reduced colonic pro-inflammatory cytokines and elevated IL-10. 16S rRNA profiling revealed that schaftoside reshaped gut microbiota composition, notably suppressing stress-enriched Bacteroides and promoting butyrate-producing Butyricicoccus. Untargeted metabolomics identified restoration of tryptophan and α-linolenic acid metabolism pathways. Spearman correlation analysis revealed significant associations between specific gut genera, fecal metabolites, and host inflammatory/neurochemical markers. Hippocampal transcriptomics indicated enrichment of cAMP signaling, dopaminergic, and serotonergic synapse pathways. Fecal microbiota transplantation (FMT) from schaftoside-treated donors partially recapitulated the behavioral, anti-inflammatory, and intestinal barrier-protective effects in antibiotic-pretreated recipient mice, accompanied by restoration of the gut microbiota and metabolite profiles. These findings demonstrate that schaftoside, the major flavonoid of fenugreek seeds, exhibits promising antidepressant-like potential through modulation of the microbiome-gut-brain axis, supporting the functional food application of fenugreek-derived flavonoids for stress-related mood disorders.
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The schizophrenia and gut microbiota: A bibliometric and visual analysis.
BACKGROUND: Many studies have explored the link between the gut microbiota and schizophrenia. To date, there have been no bibliometric analyses to summarize the association between the gut microbiota and schizophrenia. We aimed to conduct a bibliometric study of this association to determine the current status and areas for advancement in this field. MATERIALS AND METHODS: Publications related to the gut microbiota and schizophrenia were retrieved from the Web of Science Core Collection (WoSCC). The WoSCC literature analysis wire and VOSviewer 1.6.16 were used to conduct the analysis. RESULTS: In total, 162 publications were included in our study. The publications generally showed an upward trend from 2014. A total of 873 authors from 355 organizations and 40 countries/regions contributed to this field. The leading authors were Timothy Dinan, John F Cryan, and Emily Severance. The leading institutions were Johns Hopkins University, the University College Cork, and the University of Toronto. The most productive countries were the United States (US), China, and Canada. In total, 95 journals contributed to this field. Among them, the top three productive journals were Schizophrenia Research, Progress in Neuro Psychopharmacology Biological Psychiatry, and Frontiers in Psychiatry. The important keywords in the clusters were gut microbiome, bipolar disorder, schizophrenia, antipsychotics, weight gain, metabolic syndrome, gut-brain axis, autism, depression, inflammation, and brain. CONCLUSION: The main research hotspots involving the connection between schizophrenia and the gut microbiota were the characteristics of the microbiota composition in schizophrenia patients, the gut-brain axis, and microbial-based interventions for schizophrenia. The studies about the association between gut microbiota and schizophrenia are limited, and more studies are needed to provide new insights into the gut microbiota in the pathogenesis and treatment of schizophrenia.
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Influence of Environmental Factors in the Development and Outcomes of Inflammatory Bowel Disease.
Inflammatory bowel disease (IBD), which mainly comprises Crohn's disease (CD) and ulcerative colitis (UC), is a term for chronic inflammatory diseases of the gut arising due to a dysregulated immune response to a dysbiotic gut microbiome on a background of genetic predisposition. However, genetics explains a small fraction of risk, and the external environment plays a large and important role in disease pathogenesis and natural history. Cigarette smoking, one of the earliest- and most-studied risk factors, increases the risk of CD onset and is associated with severe disease. In contrast, although smoking cessation increases the risk of UC onset and relapse, current smoking appears to be protective. Appendectomy is inversely associated with the risk of UC. Various dietary factors may influence risk of IBD, including an inverse association with dietary fiber. Exclusion diets have anecdotal reports of efficacy but lack evidence from rigorous clinical trials. Psychosocial factors such as depression, stress, and sleep disturbance play a role in onset as well as in determining natural history. There is an important need for rigorous studies robustly informing the association and mechanism(s) of influence of the external environment on IBD risk and for clinical trials examining the efficacy of alteration of the environment in ameliorating the course of IBD.
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Role of Tryptophan in Microbiota-Induced Depressive-Like Behavior: Evidence From Tryptophan Depletion Study.
During the past decade, there has been a substantial rise in the knowledge about the effects of gut microbiota on host physiology and behavior, including depressive behavior. Initial studies determined that gut microbiota can regulate host tryptophan levels, which is a main serotonin precursor. A dysfunctional serotonergic system is considered to be one of the main factors contributing to the development of depression. Therefore, we hypothesized that regulation of brain tryptophan and serotonin can explain, at least partly, the effects of microbiota on depressive behavior. To test this hypothesis, we examined depressive-like behavior and brain levels of serotonin and tryptophan, of germ free (GF) and specific-pathogen free (SPF) mice under basal conditions, or after acute tryptophan depletion (ATD) procedure, which is a method to decrease tryptophan and serotonin levels in the brain. In basal conditions, GF mice exhibited less depressive-like behavior in sucrose preference, tail-suspension and forced swim tests, compared to SPF mice. In addition, in mice that were not subjected to ATD, GF mice displayed higher levels of tryptophan, serotonin and 5-hydroxyindoleacetic acid (the main degradation product of serotonin) in medial prefrontal cortex (mPFC) and hippocampus (HIPPO), compared to SPF mice. Interestingly, ATD increased depressive-like behavior of GF, but not of SPF mice. These behavioral changes were accompanied by a stronger reduction of tryptophan, serotonin and 5-hydroxyindoleacetic acid in mPFC and HIPPO in GF mice after ATD, when compared to SPF mice. Therefore, the serotonergic system of GF mice is more vulnerable to the acute challenge of tryptophan reduction, and GF mice after tryptophan reduction behave more similarly to SPF mice. These data provide functional evidence that microbiota affects depression-like behavior through influencing brain tryptophan accessibility and the serotonergic system.
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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.