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Morinda officinalis oligosaccharides ameliorate corticosterone‑induced depression‑like behaviour in mice by modulating the BDNF signalling pathway and gut microbiota.
The aim of the present study was to elucidate the regulatory effect of Morinda officinalis oligosaccharides (MOOs) on the brain‑derived neurotrophic factor (BDNF)/tropomyosin receptor kinase B (TrkB)/cAMP response element‑binding protein (CREB) signalling pathway and the gut microbiota in a corticosterone (CORT)‑induced chronic stress model. Mice received subcutaneous injections of CORT for 35 days. During this period, different concentrations of MOOs were concurrently administered by gavage. The synergistic regulatory effect of MOOs on the hippocampal BDNF/TrkB/CREB signalling pathway and gut microbiota remodelling was assessed using western blotting, ELISA, 16S ribosomal RNA sequencing, H&E/Nissl staining and reverse transcription‑quantitative PCR in the CORT‑induced chronic stress mouse model. In this model, MOOs alleviated depression‑like behaviour, promoted the expression of BDNF and neuronal nuclear antigen in the hippocampus, normalised monoamine neurotransmitter levels in the brain, activated the BDNF/TrkB/CREB signalling pathway, increased BDNF expression in the hippocampus and remodelled the intestinal microbiota, thereby exerting antidepressant effects. These results suggested that MOOs exerted antidepressant‑like effects in CORT‑exposed mice by attenuating hippocampal neuronal damage, activating the BDNF/TrkB/CREB signalling pathway and ameliorating gut microbiota dysbiosis. These findings provide novel evidence for the clinical application of MOOs in depression.
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Faecalibacterium prausnitzii, FOS and GOS loaded synbiotic reverses treatment-resistant depression in rats: Restoration of gut-brain crosstalk.
Alterations in commensal gut microbiota, such as butyrate-producing bacteria and its metabolites, have been linked to stress-related brain disorders, including depression. Herein, we investigated the effect of Faecalibacterium prausnitzii (ATCC-27766) administered along with fructooligosaccharides (FOS) and galactooligosaccharides (GOS) in a rat model of treatment-resistant depression (TRD). The behavioral changes related to anxiety-, anhedonia- and despair-like phenotypes were recorded employing elevated plus maze, sucrose-preference test, and forced-swim test, respectively. Rats exposed to unpredictable chronic mild-stress (UCMS) and adrenocorticotropic hormone (ACTH) injections exhibited a TRD-like phenotype. Six-week administration of F. prausnitzii and FOS + GOS ameliorated TRD-like conditions in rats. This synbiotic treatment also restored the decreased levels of short-chain fatty acids (SCFAs) such as acetate, propionate, and butyrate in the fecal samples of TRD rats. Synbiotic-recipient TRD rats displayed an increased abundance of Lactobacillus helveticus, Lactobacillus hamsteri, and Ruminococcus flavefaciens. Moreover, more mucus-producing goblet cells were seen in the colon of synbiotic-treated rats, suggesting improved gut health. The synbiotic treatment effectively modulated neuroinflammation by reducing proinflammatory cytokines (IFN-γ, TNF-α, CRP, and IL-6). It normalized the altered levels of key neurotransmitters such as serotonin, gamma-aminobutyric acid, noradrenaline, and dopamine in the hippocampus and/or frontal cortex. The enhanced expression of brain-derived neurotrophic factor, tryptophan hydroxylase 1, and serotonin transporter-3 (SERT-3), and reduced levels of indoleamine 2,3-dioxygenase 1 (IDO-1) and kynurenine metabolite were observed in the synbiotic-treated group. We suggest that F. prausnitzii and FOS + GOS-loaded synbiotic may reverse the TRD-like symptoms in rats by positively impacting gut health, neuroinflammation, neurotransmitters, and gut microbial composition.
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Patients with Systemic Lupus Erythematosus with Anxiety or Depression: Clinical Characteristics, Food Intake, and Gut Microbiota Profile.
BACKGROUND: Depression and anxiety are prevalent among patients with systemic lupus erythematosus (SLE), and gut microbiota may be a contributing factor. This study aimed to investigate the clinical characteristics, food intake, and gut microbiota profiles of SLE patients with anxiety or depression. METHODS: An analysis of secondary data was conducted. The primary study was conducted at Cipto Mangunkusumo Hospital, Jakarta, Indonesia, in 2017-2018. The inclusion criteria were: a diagnosis of SLE, age 18‒60 years, and gastrointestinal symptoms. The data collected included clinical data, food intake, anxiety and depression scores, SLE disease activity, and stool samples. Sequencing of the 16S rRNA gene was performed to profile the gut microbiota using DNA was extracted from the stool samples. RESULTS: After excluding those with incomplete data, 41 patients were analyzed. Among the subjects, 53.66% and 14.63% had anxiety and depression, respectively. SLE patients with anxiety were significantly more likely to harbor Bacteroides compared to those without anxiety (33.45% vs. 9.78%; p=0.02) and had lower levels of complement C3 (78.72 vs. 100.85 mg/dL; p=0.03). SLE patients with anxiety or depression had significantly lower fat intake compared to those without these conditions (38.78 vs. 48.43 g/day; p=0.04, and 31.48 vs. 45.27 g/day; p=0.04). A significant correlation was observed between the proportion of Bacteroides and SLE disease activity (p=0.02). CONCLUSION: SLE patients with anxiety showed a significantly higher proportion of Bacteroides and a lower C3 level compared to those without anxiety. Fat intake was significantly lower among SLE patients with anxiety or depression compared to those without either condition.
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Multi-Component Functionalized Bifidobacterium Longum Hydrogel for Multi-Target Integrated Therapy of Colitis-Associated Anxiety and Depression.
Inflammatory bowel diseases (IBDs) are frequently accompanied by anxiety and depression, largely driven by perturbed gut-brain axis signaling. However, current oral therapies remain constrained by the spatial and functional separation between intestinal inflammation and central nervous system dysfunction. Here, we present a comprehensive gut-brain dual region integrated therapeutic strategy based on functionalized Bifidobacterium longum hydrogel (INPs@BL@Gel), in which baicalin and tyrosine are coordinated with Fe(III) to form infinite coordination polymers (ICPs), coated with inulin, assembled onto Bifidobacterium longum (BL), and subsequently encapsulated within a pH- and matrix metalloproteinase-responsive silk fibroin-gelatin hydrogel. INPs@BL@Gel exhibits high drug-loading, effective gastric protection, inflammation-triggered release, and long-term intestinal colonization. Within the inflamed intestine, BL and components synergistically suppress inflammatory responses, restore gut microbiota homeostasis, and promote intestinal barrier repair through multi-target integrated therapy. Importantly, BL combined with components markedly enhances the production of beneficial neuroactive metabolites such as homovanillic acid and short-chain fatty acids, which integratedly regulate neuroinflammation, preserve synaptic function, and facilitate blood-brain barrier repair via the gut-brain axis. In vivo studies demonstrate that INPs@BL@Gel not only exerts potent therapeutic efficacy against colitis and effectively alleviates associated depression, but also reshapes the gut microbiota and restores barrier integrity, achieving a remarkable comprehensive therapeutic effect.
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The Association of Post-Stroke Cognitive Impairment and Gut Microbiota and its Corresponding Metabolites.
BACKGROUND: Post-stroke cognitive impairment (PSCI) is an important factor causing disabilities after acute ischemic stroke (AIS). Emerging evidence suggested that gut microbiota play an important role in cognitive impairment. OBJECTIVE: This study aimed to explore the association between PSCI and gut microbiota. METHOD: 65 patients with newly diagnostic AIS finished the fecal collection on admission and cognitive assessment 3 months later in the clinic. Fecal samples were subjected to 16SrRNA gene sequencing and gas chromatography-mass spectrometry analysis. Additionally, we enrolled new 18 AIS patients, whose treatment was supplemented by probiotics, to assess the potential of microbial treatment in PSCI. RESULTS: PSCI patients were characterized by the significantly decreased alpha-diversity, disturbed microbial composition, and corresponding metabolites compared with non-PSCI patients. Increased Fusobacterium and deficiency of microbial metabolized short-chain fatty acids (SCFAs) were significantly associated with PSCI. A model based on gut microbiota and SCFAs could predict 3 months or longer PSCI early and accurately after stroke onset. While traditional probiotic administration had little effect on PSCI, it could ameliorate patients' mood, including depression and anxiety in the 3 months after stroke. CONCLUSION: Our study revealed the association between PSCI and gut microbiota and its corresponding metabolites for the first time, suggesting the potential for applying microbiota and its corresponding metabolites to early clinical diagnosis and treatment of PSCI.
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Disturbance in human gut microbiota networks by parasites and its implications in the incidence of depression.
If you think you are in control of your behavior, think again. Evidence suggests that behavioral modifications, as development and persistence of depression, maybe the consequence of a complex network of communication between macro and micro-organisms capable of modifying the physiological axis of the host. Some parasites cause significant nutritional deficiencies for the host and impair the effectiveness of cognitive processes such as memory, teaching or non-verbal intelligence. Bacterial communities mediate the establishment of parasites and vice versa but this complexity approach remains little explored. We study the gut microbiota-parasite interactions using novel techniques of network analysis using data of individuals from two indigenous communities in Guerrero, Mexico. Our results suggest that Ascaris lumbricoides induce a gut microbiota perturbation affecting its network properties and also subnetworks of key species related to depression, translating in a loss of emergence. Studying these network properties changes is particularly important because recent research has shown that human health is characterized by a dynamic trade-off between emergence and self-organization, called criticality. Emergence allows the systems to generate novel information meanwhile self-organization is related to the system's order and structure. In this way, the loss of emergence means a depart from criticality and ultimately loss of health.
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Exploring the bidirectional causal association between Sleep Apnea Syndrome and Depression: A Mendelian randomization study involving gut microbiota, serum metabolites, and inflammatory factors.
OBJECTIVE: This study aimed to investigate the potential causal association between Sleep Apnea Syndrome (SAS) and Depression, focusing on the roles of gut microbiota, serum metabolites, and inflammatory factors in these conditions. METHODS: Mendelian Randomization (MR) analysis was performed using data from genome-wide association studies to assess 211 types of gut microbiota, 1400 serum metabolites, and 91 inflammatory factors as potential contributing factors. Causal inference was conducted using the Inverse Variance Weighted (IVW) method, with additional robustness checks through Cochran's Q test, MR-Egger regression intercept test, MR-PRESSO global test, and leave-one-out analysis. RESULTS: The MR analysis indicated a positive correlation between the risk of SAS and Depression (OR = 1.12, 95 % CI: 1.05-1.19, P < 0.001), with a reciprocal analysis showing a similar positive correlation between Depression and the risk of SAS (OR = 1.19, 95 % CI: 1.07-1.31, P = 0.001). Additionally, causal associations were identified between 15 types of gut microbiota, 36 serum metabolites, and 2 inflammatory factors with SAS, and between 11 types of gut microbiota, 23 serum metabolites, and 3 inflammatory factors with Depression (IVW, all P < 0.05). The robustness of these findings was confirmed through the MR-Egger regression intercept test and MR-PRESSO global test. CONCLUSION: This study provides epidemiological evidence of a bidirectional causal association between SAS and Depression, emphasizing the potential roles of gut microbiota, serum metabolites, and inflammatory factors in the pathogenesis of these disorders. These findings may inform the development of new therapeutic strategies.
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Exploring the Association between Anxiety, Depression, and Gut Microbiota during Pregnancy: Findings from a Pregnancy Cohort Study in Shijiazhuang, Hebei Province, China.
Negative emotions and gut microbiota during pregnancy both bear significant public health implications. However, the relationship between them has not been fully elucidated. This study, utilizing data from a pregnancy cohort, employed metagenomic sequencing to elucidate the relationship between anxiety, depression, and gut microbiota's diversity, composition, species, and functional pathways. Data from 87 subjects, spanning 225 time points across early, mid, and late pregnancy, were analyzed. The results revealed that anxiety and depression significantly corresponded to lower alpha diversity (including the Shannon entropy and the Simpson index). Anxiety and depression scores, along with categorical distinctions of anxiety/non-anxiety and depression/non-depression, were found to account for 0.723%, 0.731%, 0.651%, and 0.810% of the variance in gut-microbiota composition (p = 0.001), respectively. Increased anxiety was significantly positively associated with the abundance of Oscillibacter sp. KLE 1745, Oscillibacter sp. PEA192, Oscillibacter sp. KLE 1728, Oscillospiraceae bacterium VE202 24, and Treponema socranskii. A similar association was significantly noted for Oscillibacter sp. KLE 1745 with elevated depression scores. While EC.3.5.3.1: arginase appeared to be higher in the anxious group than in the non-anxious group, vitamin B12-related enzymes appeared to be lower in the depression group than in the non-depression group. The changes were found to be not statistically significant after post-multiple comparison adjustment.
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Diet and the gut microbiota-immune axis in the context of perinatal mental health: Protocol for a prospective cohort study.
BACKGROUND: Physiological and psychosocial changes experienced by women during the perinatal period may put them at risk for postpartum mental health disturbances. Accumulating evidence suggests that dietary patterns may influence mental health through the modulation of the gut microbiota and its effects on host immune activity. Thus, targeting the gut microbiota via dietary intake could serve as both a preventative and therapeutic strategy in improving perinatal mental health. OBJECTIVES: Here, we present a protocol for a prospective cohort study that primarily aims to determine if diet quality during pregnancy is protective against postpartum depression severity. Secondary objectives will examine if microbiota- and blood-based inflammatory markers may be associated with the relationship between prenatal diet quality and postpartum depression severity, as well as with associations between additional dietary and mental health outcomes. METHODS AND ANALYSIS: Dietary patterns and mental health symptoms will be documented in 100 pregnant women at 4 time points during pregnancy and postpartum. Participants will also provide stool and blood samples at the same time points to determine microbiota composition and predicted function and inflammatory factors, respectively. Stool microbiota will be analyzed using 16S ribosomal RNA gene sequencing and bioinformatics tools (QIIME 2/PICRUSt2). Inflammatory factors will be determined using high-sensitivity antibody-based immunoassays. Statistical analyses will include linear mixed models and hierarchical linear mixed effect models. ETHICS: The study was approved by the Research Ethics Boards of the Royal Ottawa Health Care Group (#2022002) and of the University of Ottawa (#H-06-22-8013). Informed consent will be obtained from all participants before their enrollment. DISCUSSION: Findings from this study will help develop evidence-based dietary recommendations and potential interventions for women susceptible to or suffering from postpartum mental health issues that are accessible, noninvasive, and have potential to play a role in prevention and treatment.
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A Study of Sex Differences in the Biological Pathways of Stress Regulation in Mice.
BACKGROUND: Stress is closely related to life, and it can also cause many mental disorders. However, there are significant sex differences in neuropsychiatric disorders associated with stress, particularly in depression, where the lifetime risk of depression in women is approximately twice that of men. However, the specific mechanism of this process has not been explained in detail. METHODS: Chronic restraint stress (CRS) + chronic and unpredictable mild stress (CUMS) was used to simulate social stress, and behavioral experiments, HE staining of rectal and hippocampal pathological sections, detection of depression-related biological indicators, analysis of intestinal flora diversity, and metabolomics analysis of hippocampal and intestinal contents were performed. RESULTS: The results showed that stress induced anxiety-like behavior in female mice and depression-like behavior in male mice. Sex differences in behavior may be related to monoamine neurotransmitters, hyperactivity of HPA axis, inflammatory factors, gut microbiota, and brain-gut metabolism. It is worth noting that stress caused opposite trends in DA (dopamine) levels, abundance of f-lactobaciliaceae, and levels of metabolites (1, 2-distearoyl-SN-glycero-3-phosphocholine) and PC(20:5(5Z,8Z,11Z,14Z,17Z)/20:1(11Z)) in male and female mice. CONCLUSION: The difference in neurotransmitter levels, the disorder of gut microbiota, and the abnormal brain and gut metabolism may lead to the gender difference in stress behavior.