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Lactobacillus johnsonii and 3-indolepropionic acid improve the depression-like behaviors via inhibiting neuroinflammation.
Gut microbiota-derived metabolites play a crucial role in depression. This study aimed to elucidate the role of tryptophan metabolites herein. In a CSDS mouse model, we identified eight differential species, twelve altered neurotransmitters, and two up-regulated inflammatory factors (IL-6 and IL-1β). Notably, 3-indolepropionic acid (IPA) levels were consistently reduced in feces, colon, blood, and hippocampus of CSDS mice. The decreased abundance of Lactobacillus johnsonii (L. johnsonii) was correlated closely with depression-like behaviors (DLBs), reduced fecal IPA, and elevated IL-6 and IL-1β. Both L. johnsonii and IPA supplementation alleviated DLBs, along with up-regulated AhR and down-regulated NF-κB, NLRP3, IL-6, and IL-1β in hippocampus. Moreover, both treatments significantly elevated IPA levels in peripheral and central samples, and improved the mRNA levels of AhR and NF-κB p65 in hippocampus. Critically, the antidepressant effects of L. johnsonii and IPA were counteracted by AhR antagonist CH223191. Independent experimental results showed that CH223191 had no significant effects on behaviors of CSDS mice. To our knowledge, this was the first study to report reduced IPA levels in both peripheral and central samples of CSDS mice. We also provided the first demonstration that the antidepressant effects of L. johnsonii and IPA were mediated, at least in part, through the inhibition of neuroinflammation via AhR pathway, accompanied by the restoration of IPA levels in gut-brain axis. These findings positioned L. johnsonii and IPA as promising therapeutic candidates for depression.
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The gut microbiome and diet in psychiatry: focus on depression.
PURPOSE OF REVIEW: With depressive disorders the leading source of disability globally, the identification of new targets for prevention and management is imperative. A rapidly emerging field of research suggests that the microbiome-gut-brain axis is of substantial relevance to mood and behaviour. Similarly, unhealthy diet has recently emerged as a significant correlate of and risk factor for depression. This review provides evidence for the gut microbiota as a key factor mediating the link between diet and depressive illness. RECENT FINDINGS: The development of new technologies is affording a better understanding of how diet influences gut microbiota composition and activity and how this may, in turn, influence depressive illness. New interventions are also suggesting the possible utility of pre and probiotic formulations and fermented food in influencing mental health. SUMMARY: Although in its early stages, the emerging field of research focused on the human microbiome suggests an important role for the gut microbiota in influencing brain development, behaviour and mood in humans. The recognition that the gut microbiota interacts bidirectionally with other environmental risk factors, such as diet and stress, suggests promise in the development of interventions targeting the gut microbiota for the prevention and treatment of common mental health disorders.
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Neuroprotective effect of Lactiplantibacillus plantarum Lp39-fermented milk in a murine model of depression and anxiety.
Depression and anxiety are common mental health disorders that can significantly impair quality of life. In recent years, functional foods, particularly fermented milk products, have gained attention as potential complementary therapies. Rich in probiotics and bioactive compounds, these products may help modulate the gut-brain axis, thereby improving mood and alleviating symptoms, supporting mental well-being. Hence, the potential antidepressant and anxiolytic effects of milk fermented (FM) with Lactiplantibacillus plantarum Lp39 were evaluated in a murine model. The antidepressant-like effect was assessed using unconditional behavioral tests, including the tail suspension test (TST), forced swimming test (FST), and sucrose preference test (SP). The anxiolytic-like effect was evaluated using the elevated plus maze (EPM), the light-dark box (LD), and the open field test (OFT). Additionally, oxidative stress and inflammation biomarkers were determined in the liver, plasma and hippocampus. Gut microbiota composition was also analyzed. The anxiolytic-like effect was evidenced by the OFT and LD tests. The antidepressant-like effect was demonstrated by TST and FST, along with an increased sucrose preference. FM administration significantly reduced the oxidative stress index and lipidic peroxidation and enhanced antioxidant activity in the hippocampus. Elevated IL-10 levels and lipoxygenase inhibition were observed in FM-treated animals. BNDF levels in the hippocampus were also significantly increased, and correlations were found between BNDF, oxidative stress index, IL-10, and TNF-α with SP outcomes, as well as between MDA and TNF with TST. The gut microbiota remained stable following FM consumption, while reduced Helicobacter and increased Lactobacillus populations. Weak correlations were observed between the presence of Mycoplasmataceae, Propionibacteriaceae, and Deferribacteriaceae and unconditional behavioral tests, oxidative and inflammation biomarkers. Our findings suggest that FM with Lpb. plantarum Lp39 may exert beneficial antidepressant and anxiolytic effects through neurotrophic support, anti-inflammatory and antioxidant mechanisms, without adversely affecting the gut microbiota and possibly contribute to a neuroprotective effect within the gut-brain axis.
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Gut microbiome-derived indole-3-carboxaldehyde regulates stress vulnerability in chronic restraint stress by activating aryl hydrocarbon receptors.
Chronic stress constitutes a major precipitating factor for Major Depressive Disorder (MDD), and comprehending individual differences in stress responses is crucial for the development of effective intervention strategies for MDD. Recent studies indicate that an individual's vulnerability to chronic stress is closely associated with gut microbiota composition, but the underlying mechanisms remain unclear. This study aims to investigate whether the gut microbiota and its metabolites can serve as gut-brain signaling molecules and explores how the gut microbiota affects stress sensitivity. Here, we showed that gut microbiome-derived indole-3-carboxaldehyde (I3C) can act as a gut-brain signaling molecule that links tryptophan metabolism by gut microbes to stress vulnerability in the host. First, we identified a specific reduction in gut microbiome-derived I3C levels in the hippocampus and colon through untargeted and targeted metabolomic analyses. Then, the study of gut microbiota suggested that the relative abundance of lactobacillus was reduced significantly in stress-susceptible rats, whereas fecal microbiota transplantation regulates stress vulnerability. Furthermore, supplementation with I3C and the representative I3C-producing strain, Lactobacillus reuteri, was shown to alleviate depression-like behaviors induced by chronic stress. Further research confirms that I3C can inhibit neuroinflammation and promote hippocampal neurogenesis through the aryl hydrocarbon receptors (AhR) signal pathway, thereby mitigating the host's susceptibility to stress. In conclusion, our findings elucidate that the gut microbiome-derived-I3C can help buffer the host's stress through the AhR/SOCS2/NF-κB/NLRP3 pathway, providing a gut-brain signaling basis for emotional behavior.
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Stress-induced mucin 13 reductions drive intestinal microbiome shifts and despair behaviors.
Depression is a prevalent psychological condition with limited treatment options. While its etiology is multifactorial, both chronic stress and changes in microbiome composition are associated with disease pathology. Stress is known to induce microbiome dysbiosis, defined here as a change in microbial composition associated with a pathological condition. This state of dysbiosis is known to feedback on depressive symptoms. While studies have demonstrated that targeted restoration of the microbiome can alleviate depressive-like symptoms in mice, translating these findings to human patients has proven challenging due to the complexity of the human microbiome. As such, there is an urgent need to identify factors upstream of microbial dysbiosis. Here we investigate the role of mucin 13 as an upstream mediator of microbiome composition changes in the context of stress. Using a model of chronic stress, we show that the glycocalyx protein, mucin 13, is selectively reduced after psychological stress exposure. We further demonstrate that the reduction of Muc13 is mediated by the Hnf4 transcription factor family. Finally, we determine that deleting Muc13 is sufficient to drive microbiome shifts and despair behaviors. These findings shed light on the mechanisms behind stress-induced microbial changes and reveal a novel regulator of mucin 13 expression.
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The Gut Microbiome and Mental Health: What Should We Tell Our Patients?: Le microbiote Intestinal et la Santé Mentale : que Devrions-Nous dire à nos Patients?
The gut microbiome as a potential therapeutic target for mental illness is a hot topic in psychiatry. Trillions of bacteria reside in the human gut and have been shown to play a crucial role in gut-brain communication through an influence on neural, immune, and endocrine pathways. Patients with various psychiatric disorders including depression, bipolar disorder, schizophrenia, and autism spectrum disorder have been shown to have significant differences in the composition of their gut microbiome. Enhancing beneficial bacteria in the gut, for example, through the use of probiotics, prebiotics, or dietary change, has the potential to improve mood and reduce anxiety in both healthy people and patient groups. Much attention is being given to this subject in the general media, and patients are becoming increasingly interested in the potential to treat mental illness with microbiome-based therapies. It is imperative that those working with people with mental illness are aware of the rationale and current evidence base for such treatment strategies. In this review, we provide an overview of the gut microbiome, what it is, and what it does in relation to gut-brain communication and psychological function. We describe the fundamental principles and basic techniques used in microbiome-gut-brain axis research in an accessible way for a clinician audience. We summarize the current evidence in relation to microbiome-based strategies for various psychiatric disorders and provide some practical advice that can be given to patients seeking to try a probiotic for mental health benefit.
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Probiotics alleviate depressive behavior in chronic unpredictable mild stress rat models by remodeling intestinal flora.
OBJECTIVE: To explore the effects of probiotics on depressive behavior in a chronic unpredictable mild stress (CUMS) rat model by remodeling intestinal flora. METHODS: Twenty-four male SD rats aged 6-8 weeks were randomly divided into four groups: control group, depression group (CUMS), depression+paroxetine group (Paro) and depression+probiotics group (Pro). Sucrose preference, open field and forced swimming tests were used to assess depression-like behavior in rats. ELISA was used to detect the levels of adrenocorticotropic hormone (ACTH), and corticosterone, norepinephrine and 5-hydroxytryptamine in rat serum. Real-time PCR was used to determine the changes of Lactobacillus, Bifidobacterium, Enterococcus faecalis and Escherichia coli in rat cecum. RESULTS: Compared with the control group, CUMS led to significant decreases of body weight, total traveled distance, duration in central area, immobility time, norepinephrine and 5-hydroxytryptamine contents in hippocampal tissues, as well as Lactobacillus and Bifidobacterium in the cecum. It also resulted in marked increases of the contents of E. faecalis and E. coli in the cecum, ACTH and corticosterone contents in the serum of rats. Paroxetine and probiotic treatment each diminished or prevented these changes. CONCLUSION: By remodeling intestinal flora, probiotics can reduce the CUMS-induced depressive behavior of rats, increase the levels of norepinephrine and 5-hydroxytryptamine, and inhibit the expression of ACTH and corticosterone. Significantly, the effect of both paroxetine and probiotic on microorganisms is similar.
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The gut microbiota mediates depression-like behaviors in mice with chronic Echinococcus multilocularis infection.
Alveolar echinococcosis (AE), a chronic parasitic disease caused by Echinococcus multilocularis (E. multilocularis), remains poorly characterized with respect to central nervous system (CNS) involvement, and its long-term effects on mental health have not been systematically investigated. In this study, we established a BALB/c mouse model of chronic E. multilocularis infection and applied an integrative framework combining behavioral assessments, histomorphological analyses (hematoxylin-eosin staining, Nissl staining, and transmission electron microscopy), cytometric bead array (CBA), and multi-omics approaches (16S rRNA sequencing, metagenomics, and untargeted metabolomics) to investigate infection-induced neuroimmune-gut microbiota interactions. Chronically infected mice exhibited pronounced depression-like behavioral phenotypes, accompanied by hippocampal neuronal nuclear membrane atrophy and disrupted microglial homeostasis. Both peripheral and central inflammatory profiling revealed elevated levels of pro-inflammatory mediators, particularly IL-6 and MCP-1, suggesting coordinated systemic immune activation and neuroimmune alterations. Notably, fecal microbiota transplantation (FMT) from infected donors was sufficient to induce depression-like behaviors in recipient mice, supporting a contributory role of infection-associated gut microbiota alterations in behavioral abnormalities. Integrated multi-omics analyses further revealed a marked reduction in Lactobacillus abundance in infected mice, which was positively correlated with decreased levels of key metabolites within the tryptophan/5-hydroxytryptamine (5-HT) metabolic pathway. Collectively, these findings suggest that chronic E. multilocularis infection may be associated with depression-like behaviors through gut microbiota dysbiosis and related metabolic perturbations. This study provides initial insights into the potential mechanisms underlying neuropsychiatric complications in AE and proposes a conceptual framework for future investigations into early intervention and microbiota-targeted therapeutic strategies.
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Microbial and metabolomic profiles of type 1 diabetes with depression: A case-control study.
BACKGROUND: Depression is the most common psychological disorder in patients with type 1 diabetes (T1D). However, the characteristics of microbiota and metabolites in these patients remain unclear. This study aimed to investigate microbial and metabolomic profiles and identify novel biomarkers for T1D with depression. METHODS: A case-control study was conducted in a total of 37 T1D patients with depression (TD+), 35 T1D patients without depression (TD-), and 29 healthy controls (HCs). 16S rRNA gene sequencing and liquid chromatography-mass spectrometry (LC-MS) metabolomics analysis were conducted to investigate the characteristics of microbiota and metabolites. The association between altered microbiota and metabolites was explored by Spearman's rank correlation and visualized by a heatmap. The microbial signatures to discriminate TD+ from TD- were identified by a random forest (RF) classifying model. RESULTS: In microbiota, 15 genera enriched in TD- and 2 genera enriched in TD+, and in metabolites, 14 differential metabolites (11 upregulated and 3 downregulated) in TD+ versus TD- were identified. Additionally, 5 genera (including Phascolarctobacterium, Butyricimonas, and Alistipes from altered microbiota) demonstrated good diagnostic power (area under the curve [AUC] = 0.73; 95% CI, 0.58-0.87). In the correlation analysis, Butyricimonas was negatively correlated with glutaric acid (r = -0.28, p = 0.015) and malondialdehyde (r = -0.30, p = 0.012). Both Phascolarctobacterium (r = 0.27, p = 0.022) and Alistipes (r = 0.31, p = 0.009) were positively correlated with allopregnanolone. CONCLUSIONS: T1D patients with depression were characterized by unique profiles of gut microbiota and serum metabolites. Phascolarctobacterium, Butyricimonas, and Alistipes could predict the risk of T1D with depression. These findings provide further evidence that the microbiota-gut-brain axis is involved in T1D with depression.
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The gut-brain axis and inflammatory mediators in suicide and mental disorders with high suicide rates: a review of current evidence.
The interplay between gastrointestinal microbiota and mental disorders has recently been spotlighted. This review investigated discrete evidence suggesting associations between the gastrointestinal microbiome and inflammation with suicide. Fusicatenibavter, Hungatella, Veillonella, and Megasphaera have positive associations, but Clostridium, Butyricicoccus, Desulfovibrio piger, and Parabacteroides merdae have negative associations with suicidality. Additionally, lower species uniformity index, higher intestinal fatty acid binding protein secretion, lower zonulin secretion, higher interleukin-6 in cerebrospinal fluid, and laxative abuse are associated with suicidality. As nearly 90% of suicides occur in patients with mental disorders, the interaction between the gut microbiota and inflammation with these disorders together was also documented. Regarding this, major depressive disorder, psychosis and schizophrenia, generalised anxiety disorder, and substance use disorder were investigated. Bacteroidetes and Firmicutes show prominent changes in most cases. In addition, gut bacterial and non-bacterial microbiome alterations and subsequent dysbiosis may contribute to inflammation, in which cytokines affect microglial activity. Meanwhile, impaired intestinal homeostasis may influence these disorders through the vagus nerve, the hypothalamus-pituitary-adrenal axis, and the kynurenine pathway. Beyond these, direct effects of the gut microbiome on immunity are being hypothesised. In conclusion, the gut microbiota imbalance may influence the nervous system environment from non-inflammatory to inflammatory caused by pro-inflammatory cytokine influx into the brain. Consequently, microbiota imbalances may be associated with mental disorders. Specifically, limited evidence indicated possible links between microbiome alterations and suicide, highlighting the need for further research clarifying these associations and underpinning mechanisms. Other factors, including genetic vulnerability, environmental influences, and neurochemical pathways, should also be considered.