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Paeonia lactiflora Pall. Polysaccharide alleviates depression in CUMS mice by inhibiting the NLRP3/ASC/Caspase-1 signaling pathway and affecting the composition of their intestinal flora.
ETHNOPHARMACOLOGICAL RELEVANCE: Paeonia lactiflora Pall. (PL) has been commonly used to de-stressing the liver and relieve depression in traditional Chinese medicine for over a thousand years. Recently, it has been widely used in studies on anti-depressant, anti-inflammatory and regulation of intestinal flora. However, the polysaccharide component has received less attention than the saponin component of PL. AIM OF THE STUDY: This study aimed to elucidate the effects of Paeonia lactiflora polysaccharide (PLP) on depressive behavior in mice in a chronic unpredictable mild stress (CUMS) model and its possible action mechanisms. MATERIALS AND METHODS: A model of chronic depression induced by the CUMS approach. Behavioral experiments were used to assess the success of the CUMS model and the therapeutic impact of PLP. Then the extent of damage to the colonic mucosa was assessed by H&E staining; the extent of neuronal damage was assessed by Nissler staining. Inflammatory factor expression was assessed at different sites in the mouse by enzyme-linked immunoassay (Elisa). The alterations of faecal microflora were detected by 16S rRNA gene sequencing. In the colonic tissues, NLRP3, ASC and Caspase-1 mRNA and protein levels detected by quantitative real-time PCR (qRT-PCR) and Western blot(WB). RUSULTS: PLP can improve depressive behavior in CUMS mice, and colonic mucosal and neuronal damage. Elisa assay showed that PLP could reduce interleukin-1β (IL-1β), interleukin-6 (IL-6), tumour necrosis factor-α (TNF-α) levels, and increase 5-Hydroxytryptamine(5-HT) levels in CUMS mice. 16S sequencing analysis showed that PLP could regulate the intestinal flora of CUMS mice and increase their species richness. In addition, PLP significantly inhibited NLRP3/ASC/Caspase-1 signalling pathways activation in the colonic tissues of CUMS mice. CONCLUSIONS: PLP modulates depression-related intestinal ecological dysregulation, increases species richness, and inhibits inflammatory factors levels and NLRP3 inflammasome activation to reduce colonic mucosal and neurons damage, thereby improving depression-like behavior and neurotransmitter release in CUMS mice.
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The Microbiome-Brain Axis in Burning Mouth Syndrome and Its Comorbidities: An Integrated Perspective.
Burning mouth syndrome (BMS) is a chronic nociplastic pain condition of unknown etiology, predominantly affecting women and highly comorbid with depression and anxiety. This narrative review proposes a comprehensive model integrating the significant role of the oral and intestinal microbiomes in BMS pathology. We explore how microbial dysbiosis compromises barrier functions, leading to systemic and neuroinflammation, and subsequently modulates key brain networks involved in pain processing and emotional regulation. Evidence suggests that dysbiosis within the oral microbiome (e.g., increased Streptococcus, Rothia, Bergeyella, Granulicatella, Neisseria) and/or the intestinal microbiome contributes to BMS pathology. This dysbiosis can compromise oral and intestinal barrier functions, leading to the systemic dissemination of bacterial components and inflammatory mediators. These factors induce neuroinflammation, which directly influences and dysregulates key brain networks such as the default mode network and salience network, crucial for pain processing and emotional regulation. The vagus nerve serves as a critical bidirectional communication pathway within this axis. Preliminary studies indicate potential therapeutic benefits of probiotics (e.g., Lactobacillus reuteri in BMS), but large-scale evidence is still emerging. The pathology of BMS, intertwined with depression and anxiety, can be significantly influenced by the oral and intestinal microbiomes. Dysbiosis contributes to chronic systemic and neuroinflammation, driving maladaptive changes in brain networks and neurotransmitter systems. While promising, the field is nascent, requiring further causal studies, detailed mechanistic insights, and robust clinical trials to establish the full therapeutic potential of microbiome-targeted interventions.
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High-fat diet induces depression-like behaviour in mice associated with changes in microbiome, neuropeptide Y, and brain metabolome.
Objectives: The biological mechanisms linking diet-related obesity and depression remain unclear. Therefore, we examined the impact of high-fat diet (HFD) on murine behaviour, intestinal microbiome, brain metabolome, neuropeptide Y (NPY) expression, and dipeptidyl peptidase-4 (DPP-4) activity.Methods: Male C57Bl/6J mice were fed an HFD (60 kJ% from fat) or control diet (12 kJ% from fat) for 8 weeks, followed by behavioural phenotyping. Caecal microbiome was analysed by 16S rDNA sequencing, brain metabolome by 1H nuclear magnetic resonance, NPY expression by PCR and immunoassay, and dipeptidyl peptidase-4 (DPP-4) activity by enzymatic assay. The effect of a 4-week treatment with imipramine (7 mg/kg/day) and the DPP-4 inhibitor sitagliptin (50 mg/kg/day) on HFD-induced behavioural changes was also tested.Results: HFD led to a depression-like phenotype as revealed by reduced sociability and sucrose preference. In the caecum, HFD diminished the relative abundance of Bacteroidetes and increased the relative abundance of Firmicutes and Cyanobacteria. In the brain, HFD modified the metabolome of prefrontal cortex and striatum, changing the relative concentrations of molecules involved in energy metabolism (e.g. lactate) and neuronal signalling (e.g. γ-aminobutyric acid). The expression of NPY in hypothalamus and hippocampus was decreased by HFD, whereas plasma NPY and DPP-4-like activity were increased. The HFD-induced anhedonia remained unaltered by imipramine and sitagliptin.Discussion: The depression-like behaviour induced by prolonged HFD in mice is associated with distinct alterations of intestinal microbiome, brain metabolome, NPY system, and DPP-4-like activity. Importantly, the HFD-evoked behavioural disturbance remains unaltered by DPP-4 inhibition and antidepressant treatment with imipramine.
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Effects of berberine on a rat model of chronic stress and depression via gastrointestinal tract pathology and gastrointestinal flora profile assays.
Chronic stress and depression are challenging conditions to treat, owing to their complexity and lack of clinically available and effective therapeutic agents. The aim of the present study was to investigate the mechanism by which berberine acts, by examining alterations to gastrointestinal tract histopathology and flora profile in a rat model, following the induction of stress. Research associating gastrointestinal flora and depression has increased, thus, the present study hypothesized that stress induces depression and changes in the gastrointestinal system. The chronic mild stress rat model was previously established based on a set of 10 chronic unpredictable stress methods. In the present study, the measurements of body weight, behavior, gastrointestinal tract histopathology and gastrointestinal flora profile were collected in order to elucidate understanding of chronic stress and depression in this region. In the present study, induced stress and the resulting depression was demonstrated to significantly decrease the body weight and sucrose preference of rats, as well as significantly increasing traverse time, vertical movement time, grooming time and motionless time in an open‑field test. Following modeling and subsequent treatment with low or high doses of berberine, the measurements were significantly different when compared with unstressed rats. Berberine appears to reverse the physical damage brought about by stress within the gastric mucosa and intestinal microvilli of the stomach, ileum, cecum and colon. Using enterobacterial repetitive intergenic consensus sequence‑based polymerase chain reaction analysis, several distinctive bands disappeared following modeling; however, novel distinctive bands appeared in response to the graded berberine treatment. In conclusion, the present study identified that high concentrations of berberine markedly protects rats from various symptoms of chronic stress and depression, with the potential of facilitating treatment within clinical practice.
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Lactiplantibacillus plantarum as a promising adjuvant for neurological disorders therapy through the brain-gut axis and related action pathways.
Dysbiosis in neurological disorders has highlighted the gut-microbiota-brain axis and psychobiotics and their ability to act on the brain-gut axis. Studying and discovering new approaches in therapies for neuropsychiatric disorders are strategies that have been discussed and put into practice. Lactiplantibacillus plantarum is a lactic acid bacteria species with an extensive history of safe use whose action as a psychobiotic has been successfully explored. This review describes and discusses the mechanisms of action of L. plantarum and its potential for the prevention and treatment of neurological disorders. Randomized and controlled trials in humans or animals and using supplements based on different strains of L. plantarum were selected. The psychobiotic effect of L. plantarum has been shown, mainly through its action on the Hypothalamic-Pituitary-Adrenal (HPA) axis and regulation of levels of pro-inflammatory cytokines. Furthermore, it could protect the integrity of the intestinal barrier and decrease inflammation, alleviating a series of symptoms of neurological diseases. The results showed improvements in cognitive function, memory, anxiety, hyperactivity, Attention Deficit Hyperactivity Disorder (ADHD), sleep quality, and growth stimulation of beneficial species of bacteria in the gut. Larger and deeper studies are needed to use psychobiotics to prevent and treat neurological disorders.
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Fecal microbiota transplantation alleviates mild-moderate COVID-19 associated diarrhoea and depression symptoms: A prospective study of a randomized, double-blind clinical trial.
Currently, the emergence of the endemic Coronavirus disease (COVID-19) situation still poses a serious threat to public health. However, it remains elusive about the role of fecal microbiota transplantation in treating COVID-19. We performed a randomized, double-blind, placebo-controlled clinical trial enrolling a cohort of 40 COVID-19 patients with mild-moderate symptoms. Our results showed that fecal microbiota transplantation provided an amelioration in diarrhoea (p = 0.026) of digestive system and depression (p = 0.006) of neuropsychiatric-related symptom in COVID-19 patients, respectively. Meanwhile, we found that the number of patients with diarrhoea decreased from 19 to 0 on day 7 after fecal microbiota transplantation treatment, and it was statistically changed compared to the placebo group (p = 0.047). Of note, the serum concentration of aspartate aminotransferase-to-alanine aminotransferase ratio (AST/ALT, fecal microbiota transplantation, pre vs. post: 0.966 vs. 0.817), a biomarker for predicting long COVID-19, was significantly reduced by fecal microbiota transplantation. In all, our study supports that fecal microbiota transplantation could be a novel therapeutic strategy for COVID-19 patients with diarrhoea and depressive symptoms, which is potentially valuable in ameliorating long COVID-19 symptoms.
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Multi-Probiotics ameliorate Major depressive disorder and accompanying gastrointestinal syndromes via serotonergic system regulation.
INTRODUCTION: Major depressive disorder (MDD) is a leading global psychiatric disease. MDD is highly comorbid with gastrointestinal abnormalities, such as gut motility dysfunction. An effective strategy to manage depression and its accompanying gastrointestinal symptoms is warranted. OBJECTIVES: Three probiotic strains (Bifidobacterium breve CCFM1025, Bifidobacterium longum CCFM687, and Pediococcus acidilactici CCFM6432) had previously been validated in mice to possess antidepressant-like potential. This study investigated the potential psychotropic effects of a combined three-strain probiotic intervention for human MDD patients. The mechanism of action was further investigated in the stress-induced depression mice model. METHODS: MDD patients were given a freeze-dried, mixed probiotic formula for four weeks. The patients' psychometric and gastrointestinal conditions were evaluated using clinical rating scales before and after treatment. Their gut microbiome was also analysed using 16S rRNA gene amplicon sequencing. The mechanisms underlying the beneficial probiotic effects were determined using a chronic stress-induced depressive mouse model. RESULTS: Multi-probiotics significantly reduced depression scores, and to a greater extent than the placebo (based on the Hamilton Depression Rating, Montgomery-Asberg Depression Rating, and Brief Psychiatric Rating Scales). Multi-probiotics also significantly improved the patients' gastrointestinal functions (based on self-evaluation using the Gastrointestinal Symptom Rating Scale). Serotonergic system modification was demonstrated as the key mechanism behind the probiotics' benefits for the brain and the gut. CONCLUSION: Our findings suggest a novel and promising treatment to manage MDD and accompanying gut motility problems, and provide options for treating other gut-brain axis-related disorders.
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We are not Alone in Our Body: Insights into the Involvement of Microbiota in the Etiopathogenesis and Pharmacology of Mental Illness.
BACKGROUND: The etiopathogenesis of psychiatric disorders is still not completely understood. Growing evidence supports the hypothesis that mental illness and related disturbances do not necessarily originate in the brain. Inflammation has been suggested to play a central role in psychiatric disorders and altered levels of peripheral cytokines have been reported in several studies. Recently, it has emerged that bacteria populating the human gut could modulate low-grade inflammation, as well as high-order brain functions, including mood and behavior. These bacteria constitute the microbiota, a large population comprising 40,000 bacterial species and 1,800 phila involved in key processes important to maintain body homeostasis. METHOD: In this review, we present and discuss studies exploring the role of dysbiosis and products of the gutmicrobiota in the pathogenesis of psychiatric disorders, as well as their potential involvement in mediating the effect of antidepressants, mood stabilizers, and antipsychotics. RESULTS: Although this field is still at its early stage of development, a growing number of studies suggest that an altered composition of the gut microbiota, together with translocation of bacterial products into the systemic circulation, might play a role in the pathogenesis of psychiatric disorders as well as in response to psychotropic medications. CONCLUSION: An altered composition and functioning of gut microbiota have been reported in psychiatric disorders, and recent findings suggest that gut bacteria could be involved in modulating the efficacy of psychotropic medications.
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Inflammatory bowel disease and neuropsychiatric disorders: Mechanisms and emerging therapeutics targeting the microbiota-gut-brain axis.
Crohn's disease (CD) and ulcerative colitis (UC) are the two major entities of inflammatory bowel disease (IBD). These disorders are known for their relapsing disease course and severe gastrointestinal symptoms including pain, diarrhoea and bloody stool. Accumulating evidence suggests that IBD is not only restricted to the gastrointestinal tract and that disease processes are able to reach distant organs including the brain. In fact, up to 35 % of IBD patients also suffer from neuropsychiatric disorders such as generalized anxiety disorder and major depressive disorder. Emerging research in this area indicates that in many cases these neuropsychiatric disorders are a secondary condition as a consequence of the disturbed communication between the gut and the brain via the microbiota-gut-brain axis. In this review, we summarise the current knowledge on IBD-associated neuropsychiatric disorders. We examine the role of different pathways of the microbiota-gut-brain axis in the development of CNS disorders highlighting altered neural, immunological, humoral and microbial communication. Finally, we discuss emerging therapies targeting the microbiota-gut-brain axis to alleviate IBD and neuropsychiatric symptoms including faecal microbiota transplantation, psychobiotics, microbial metabolites and vagus nerve stimulation.
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Does Improving Depression Symptoms in Young Adults With Inflammatory Bowel Disease Alter Their Microbiome?
BACKGROUND: Patients with inflammatory bowel diseases (IBDs) are more likely to have depression and anxiety symptoms compared with healthy individuals and those with other chronic illnesses. Previous studies have shown a link between the microbiome composition and depression symptoms; however, many antidepressant medications have antibacterial activity confounding cross-sectional studies of these populations. Therefore, we aimed to determine whether we could detect longitudinal changes in the microbiome of a subset of patients who participated in a previously published mindfulness-based cognitive therapy (MBCT) study to improve depression symptoms in adolescents and young adults with IBD. METHODS: Stool samples were collected at baseline and 8 weeks (n = 24 participants, 37 total samples, 13 paired samples). During this time, some participants achieved a 50% reduction in their depression symptoms either through MBCT or treatment as usual with their mental health team (responders). The microbiome composition and function of responders were compared with participants who did not improve their depression scores (nonresponders). Depression scores were determined using the depression, anxiety, and stress score (DASS-21), and metagenomic sequencing of stool samples was performed. RESULTS: No difference in alpha diversity was found between responders and nonresponders. Beta diversity measures were similarly unchanged. Clinical features including fecal calprotectin, C-reactive protein, and serum IL-6 levels were unchanged. CONCLUSIONS: In this small longitudinal study, we were not able to detect longitudinal changes in the microbiome associated with improvement in depression scores. Follow-up studies that are sufficiently powered to detect changes in the microbiome are required to confirm our results.