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Unlocking the Link Between Gut Microbiota and Psychopathological Insights in Anorexia Nervosa: A Systematic Review.
OBJECTIVE: This systematic review explores the associations between qualitative/quantitative changes in gut microbiota and psychopathological symptoms or other clinical features in patients with eating disorders (EDs). Secondary outcomes include exploring gut microbiota changes in EDs and potential relationships with psychotropic drug use. METHOD: A systematic search was conducted across biomedical databases from inception to June 2024 according to PRISMA guidelines. The risk of bias was assessed, and a narrative synthesis was performed due to the heterogeneity of the outcomes. RESULTS: Only findings related to anorexia nervosa (AN) were identified. Ten studies, of which seven were longitudinal, two cross-sectional, and one interventional (N = 350 patients with AN, and 304 HCs), were included. Despite no clear links between diversity metrics and clinical symptoms being observed, specific taxa belonging to phylum Firmicutes, such as Clostridium, Roseburia, Lactobacillus, Faecalibacterium, and Bifidobacterium belonging to Actinobacteriota correlated with ED psychopathology, including anxiety and depressive symptoms. CONCLUSIONS: Changes in microbiota were related to anxiety and depressive symptoms, as well as altered eating behaviours by modulating inflammation and insulin pathways through short-chain fatty acids (SCFAs), that also lead to neurotransmitter imbalances. Further studies are required to replicate these finding and to explore whether similar patterns are observed in other EDs.
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Akkermansia muciniphila-derived SCFAs improve the depression-like behaviors of mice by inhibiting neuroinflammation.
This study was conducted to explore the effects of Akkermansia muciniphila (A. muciniphila) on depression and its underlying molecular mechanisms. Using data from our previous work, we found that the relative abundance of A. muciniphila might be lower in depressed subjects compared to control subjects. Then, using chronic restraint stress (CRS) depression model, we found that mice with depression-like behaviors had significantly disordered gut microbiota, lower short-chain fatty acids (SCFAs) levels (in both feces and serum) and higher inflammation levels in the hippocampus. After A. muciniphila intervention, depression-like behaviors were significantly improved, along with the improved gut microbiota compositions in mice with depression-like behaviors. Meanwhile, the increased SCFAs levels (in both feces and serum), increased free fatty acid receptors 2 (FFAR2) in hippocampus and decreased inflammation levels (in hippocampus) were observed in mice with depression-like behaviors receiving A. muciniphila. We also found that FFAR2 antagonist could counteract the antidepressant effects of A. muciniphila. Our results suggested that A. muciniphila could improve depression-like behaviors by regulating inflammation levels via gut microbiota-derived SCFAs, and SCFAs-FFAR2-NF-κB-NLRP3-IL-6/IL-1β pathway might be a potential pathway in this process.
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Targeting NEK7 modulates pyroptosis and gut microbiota to alleviate depression-like behavior in rats.
NIMA-associated kinase 7 (NEK7) is a serine/threonine kinase that regulates the aberrant activation of the inflammasome of NOD-like receptor thermal protein domain associated protein 3 (NLRP3), which leads to inflammatory diseases. Depression, a prevalent psychiatric condition, has been linked to neuroinflammatory processes. However, the precise molecular and cellular mechanisms underlying the role of NEK7 in depression pathogenesis remain incompletely characterized. Our study demonstrated elevated NEK7 expression in the hippocampus of maternal separation (MS) and chronic unpredictable mild stress (CUMS)-induced depressed rats. Adeno-associated virus (AAV)-mediated delivery of shNEK7 effectively alleviated depression-like behavioral deficits, downregulated pyroptosis marker protein expression, reduced inflammatory cytokine levels (interleukin-1β and interleukin-18), and preserved neuronal survival and cellular structure. Furthermore, hippocampal NEK7 knockdown restored gut microbiota homeostasis in depression-like rats, particularly affecting the relative abundance of Corynebacterium and Prevotella genera. Notably, for the first time, the metabolite corynoxine was found to be associated with hippocampal NEK7 knockdown in depression-like rats. Taken together, our results reveal that NEK7 may be a promising target for the treatment of depression and provide new experimental evidence for clinical application.
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The effect of exercise on depression and gut microbiota: Possible mechanisms.
Exercise can effectively prevent and treat depression and anxiety, with gut microbiota playing a crucial role in this process. Studies have shown that exercise can influence the diversity and composition of gut microbiota, which in turn affects depression through immune, endocrine, and neural pathways in the gut-brain axis. The effectiveness of exercise varies based on its type, intensity, and duration, largely due to the different changes in gut microbiota. This article summarizes the possible mechanisms by which exercise affects gut microbiota and how gut microbiota influences depression. Additionally, we reviewed literature on the effects of exercise on depression at different intensities, types, and durations to provide a reference for future exercise-based therapies for depression.
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The pharmacological actions of Danzhi-xiaoyao-San on depression involve lysophosphatidic acid and microbiota-gut-brain axis: novel insights from a systems pharmacology analysis of a double-blind, randomized, placebo-controlled clinical trial.
Danzhi-xiaoyao-San (DZXYS), a Traditional Chinese Medicine, plays an essential role in the clinical treatment of depression, but its mechanisms in humans remain unclear. To investigate its pharmacological effects and mechanisms as an add-on therapy for depression, we conducted a double-blind, placebo-controlled trial with depressed patients receiving selective serotonin reuptake inhibitors (SSRIs). Serum and fecal samples were collected for metabolomic and microbiome analysis using UHPLC-QTRAP-MS/MS and 16S rRNA gene sequencing technologies, respectively. Depression symptoms were assessed using the 24-item Hamilton Depression Scale. We employed network pharmacology, metabolomics, and molecular docking to identify potential targets associated with DZXYS. We also examined the correlation between gut microbes and metabolites to understand how DZXYS affects the microbiota-gut-brain axis. The results showed that DZXYS combined with SSRIs was more effective than SSRIs alone in improving depression. We identified 39 differential metabolites associated with DZXYS treatment and found seven upregulated metabolic pathways. The active ingredients quercetin and luteolin were docked to targets (AVPR2, EGFR, F2, and CDK6) associated with the enriched pathways 'pancreatic cancer' and 'phospholipase D signaling pathway', which included the metabolite lysophosphatidic acid [LPA(0:0/16:0)]. Additionally, we identified 32 differential gut microbiota species related to DZXYS treatment, with Bacteroides coprophilus and Ruminococcus gnavus showing negative correlations with specific metabolites such as L-2-aminobutyric acid and LPA(0:0/16:0). Our findings indicate that DZXYS's antidepressant mechanisms involve multiple targets, pathways, and the regulation of LPA and the microbiota-gut-brain axis. These insights from our systems pharmacology analysis contribute to a better understanding of DZXYS's potential pharmacological mechanisms in depression treatment.Communicated by Ramaswamy H. Sarma.
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Psychobiotic Lactobacillus plantarum JYLP-326 relieves anxiety, depression, and insomnia symptoms in test anxious college via modulating the gut microbiota and its metabolism.
INTRODUCTION: Test anxiety is a common issue among college students, which can affect their physical and psychological health. However, effective interventions or therapeutic strategies are still lacking. This study aims to evaluate the potential effects of Lactobacillus plantarum JYLP-326 on test anxious college students. METHODS: Sixty anxious students were enrolled and randomly allocated to the placebo group and the probiotic group. Both groups were instructed to take placebo and JYLP-326 products twice per day for three weeks, respectively. Thirty unanxious students with no treatments were assigned to a regular control group. The anxiety, depression, and insomnia questionnaires were used to measure students' mental states at the baseline and the end of this study. 16S rRNA sequencing and untargeted metabolomics were performed to analyze the changes in the gut microbiota and fecal metabolism. RESULTS: The questionnaire results suggested that JYLP-326 administration could relieve the symptoms of anxiety, depression, and insomnia in test anxious students. The gut microbiomes of the placebo group showed a significantly greater diversity index than the control group (p < 0.05). An increased abundance of Bacteroides and Roseburia at the genus level was observed in the placebo group, and the relative abundance of Prevotella and Bifidobacterium decreased. Whereas, JYLP-326 administration could partly restore the disturbed gut microbiota. Additionally, test anxiety was correlated with disordered fecal metabolomics such as a higher Ethyl sulfate and a lower Cyclohexylamine, which could be reversed after taking JYLP-326. Furthermore, the changed microbiota and fecal metabolites were significantly associated with anxiety-related symptoms. CONCLUSION: The results indicate that the intervention of L. plantarum JYLP-326 could be an effective strategy to alleviate anxiety, depression, and insomnia in test anxious college students. The potential mechanism underlying this effect could be related to the regulation of gut microbiota and fecal metabolites.
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Chronic chlorpyrifos exposure induced depression and anxiety by gut microbiota alterations combined with metabolic disorders of ammonia and quinolinate.
The potential neurotoxicity associated with chronic exposure to chlorpyrifos (CPF) raises significant concerns, since its safe exposure dose estimated from the past toxicological data are questionable. CPF is frequently detected in environmental samples, but the reference data on chronic exposure at environmentally relevant concentrations remains scarce. Herein, a 30-week mouse model was exposed to CPF at 10 and 100 μg/L in drinking water and found to exhibit significant anxiety-like and depressive-like behaviors at 100 μg/L. Through 16S rRNA sequencing and untargeted metabolomics, chronic CPF exposure was observed to reduce bacterial diversity, increase Prevotellaceae and Clostridiaceae and decrease Lactobacillus. These alterations in the gut microbiota (GM) contributed to inflammatory environmental in the colon, which disrupted ammonia and tryptophan metabolism, ultimately leading to the accumulation of glutamate and quinolinate in brain. Alterations in GM and metabolites were correlated and exhibited a dose-dependent relationship with CPF. Treatments with antibiotics, ammonia and quinolinate confirmed that synchronous metabolic disorders were responsible for inducing depression in mice, which was linked to GM alterations induced by CPF exposure. This study aims to highlight to the adverse effects of pesticide residues on public mental health and advance understanding of the toxicity mechanism associated with low-dose CPF.
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The Intersection between Tryptophan-Kynurenine Pathway Metabolites and Immune Inflammation, Hormones, and Gut Microbiota in Perinatal Depression.
Perinatal depression is a prevalent mental disorder among pregnant women, characterized by sleep disturbances, appetite changes, negative emotions, cognitive impairment, and suicidal or homicidal tendencies. These symptoms severely compromise personal well-being, disrupt family life, and burden society. Early detection and intervention are thus crucial. The tryptophan-kynurenine (TRP-KYN) pathway is central to the inflammatory hypothesis of depression and has gained significant attention in perinatal depression research. This pathway encompasses numerous metabolic enzymes and neuroactive metabolites that interact with other physiological systems, influencing neurotransmitter synthesis and neuronal development. Through these interactions, the TRP-KYN pathway exerts psychotropic effects. This article reviews the key metabolites and enzymes of the TRP-KYN pathway and examines its intersection with immune inflammation, hormones, and gut microbiota.
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Absence of gut microbiota influences lipopolysaccharide-induced behavioral changes in mice.
Changes in the microbiota composition of gastrointestinal tract are emerging as potential players in the physiopathology of neuropsychiatric disorders. In the present work we evaluated the relationship between the absence of gut microbiota and neuroinflammatory mechanisms in a murine model of LPS-induced behavioral alterations. Germ-free (GF) or conventional male mice received a single i.p. injection of lipopolysaccharide (LPS i.p.; 0.83mg/Kg) or PBS, and after 24h they were tested for depressive-like behaviors (forced swimming test, tail suspension test - TST, or sucrose preference test - SPT). After behavioral evaluation, animals were analyzed for possible changes in neuroplasticity by means of BDNF, NGF and cytokines levels in prefrontal cortex and hippocampus, and the expression of Iba-1 (microglial activation marker) in the hippocampus, and the cellular activity marker, ΔFosB, in the dorsal raphe nucleus. In conventional mice, LPS induced depressive-like behaviors. LPS-induced changes were followed by up-regulation of the expression of TNF and Iba-1 in the hippocampus. The same effects were not observed in GF mice. Behavioral effects of LPS were not observed in GF mice submitted to TST. GF mice present a lower response to the anhedonia-like effect induced by LPS when compared to conventional animals (SPT). There was up-regulation of ΔFosB in the dorsal raphe nucleus in the absence of gut microbiota, events not influenced by LPS treatment. Our results suggest that gut-microbiota interactions influence depressive-like behaviors, raphe nucleus activation and activation of pro-inflammatory mechanisms within the hippocampus.
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The outer membrane protein Amuc_1100 of Akkermansia muciniphila alleviates the depression-like behavior of depressed mice induced by chronic stress.
Akkermansia muciniphila is a symbiotic intestinal bacterium with a high medicinal value. Amuc_1100 is the outer membrane protein of A. muciniphila and plays an important role in the interaction between A. muciniphila and its host. The objective of this study was to evaluate the antidepressant activity of Amuc_1100 in a chronic unpredictable mild stress (CUMS) model. Amuc_1100 intervention ameliorated CUMS-induced depression-like behavior and CUMS-induced down-regulation of serotonin (5-hydroxytryptamine, or simply, 5-HT) in the serum and colon of mice. Microbial analysis of mouse feces showed that Amuc_1100 could improve the gut microbiota dysregulation induced by CUMS. In addition, Amuc_1100 intervention could also improve the down-regulation of brain-derived neurotrophic factor (BDNF) and inflammation in the hippocampus induced by CUMS. These results suggest that Amuc_1100 has a good antidepressant effect, and the mechanism may be related to the improvement of gut microbiota, the up-regulation of the BDNF level, and the inhibition of the neuroinflammatory response.