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Anxiety, Depression, and the Microbiome: A Role for Gut Peptides.
The complex bidirectional communication between the gut and the brain is finely orchestrated by different systems, including the endocrine, immune, autonomic, and enteric nervous systems. Moreover, increasing evidence supports the role of the microbiome and microbiota-derived molecules in regulating such interactions; however, the mechanisms underpinning such effects are only beginning to be resolved. Microbiota-gut peptide interactions are poised to be of great significance in the regulation of gut-brain signaling. Given the emerging role of the gut-brain axis in a variety of brain disorders, such as anxiety and depression, it is important to understand the contribution of bidirectional interactions between peptide hormones released from the gut and intestinal bacteria in the context of this axis. Indeed, the gastrointestinal tract is the largest endocrine organ in mammals, secreting dozens of different signaling molecules, including peptides. Gut peptides in the systemic circulation can bind cognate receptors on immune cells and vagus nerve terminals thereby enabling indirect gut-brain communication. Gut peptide concentrations are not only modulated by enteric microbiota signals, but also vary according to the composition of the intestinal microbiota. In this review, we will discuss the gut microbiota as a regulator of anxiety and depression, and explore the role of gut-derived peptides as signaling molecules in microbiome-gut-brain communication. Here, we summarize the potential interactions of the microbiota with gut hormones and endocrine peptides, including neuropeptide Y, peptide YY, pancreatic polypeptide, cholecystokinin, glucagon-like peptide, corticotropin-releasing factor, oxytocin, and ghrelin in microbiome-to-brain signaling. Together, gut peptides are important regulators of microbiota-gut-brain signaling in health and stress-related psychiatric illnesses.
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Phytotherapy and the Role of Bioactive Compounds in Modulating Mechanisms of Overweight and Obesity Comorbid with Depressive Symptoms-A Scoping Review of Mechanisms of Action.
Obesity and depression frequently coexist, sharing overlapping molecular pathways such as inflammation, oxidative stress, gut microbiota dysbiosis, and neuroendocrine dysfunction. Recent research highlights the therapeutic potential of plant-derived bioactive compounds in targeting these shared mechanisms. This scoping review followed Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines and included 261 peer-reviewed studies identified through PubMed, Scopus, and the Web of Science up to December 2024. Studies were screened based on predefined inclusion and exclusion criteria. This review synthesizes data from peer-reviewed studies, including both preclinical and clinical investigations, focusing on polyphenols, flavonoids, alkaloids, and other phytochemicals with anti-inflammatory, antioxidant, neuroprotective, and metabolic effects. Compounds such as quercetin, epigallocatechin gallate (EGCG), resveratrol, curcumin, anthocyanins, and luteolin demonstrate promise in modulating adenosine monophosphate-activated protein kinase (AMPK), brain-derived neurotrophic factor (BDNF), nuclear factor kappa B (NF-κB), and gut-brain axis pathways. Our scoping review, conducted in accordance with PRISMA guidelines, identifies promising combinations and mechanisms for integrative phytotherapy. These findings underscore the potential of botanical strategies in developing future interventions for metabolic and mood comorbidities.
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The gut reaction to couples' relationship troubles: A route to gut dysbiosis through changes in depressive symptoms.
The gut microbiota plays a role in a wide range of diseases and disorders, with low microbial diversity and richness emerging as notable risk factors. This longitudinal study addressed the impact of marital quality (assessed by the Couples Satisfaction Index) on changes in depressive symptoms, and gut diversity, richness, and permeability. On two occasions an average of 90 days apart, 162 people provided stool and blood samples, and completed questionnaires. Depressive symptoms, assessed by the Center for Epidemiological Studies Depression Scale (CES-D), increased from visit 1 to visit 2 in those with clinically significant relationship problems, in contrast to the lack of change among their more satisfied counterparts. These changes in depression were consequential: the gut microbiota's diversity and richness decreased in tandem with the increase in depressive symptoms. Lower relationship satisfaction also foreshadowed increases in lipopolysaccharide binding protein from visit 1 to visit 2, reflecting greater translocation of bacterial endotoxin from the gut to blood circulation, a process that fuels inflammation. Lower diversity and richness provide a pathway from depressive symptoms and marital distress to subsequent health risk.
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Alteration of colonic circadian rhythm by gut microbiota dysbiosis and SCFA reduction links chronic stress-induced depressive-like behavior.
BACKGROUND: Chronic stress partially leads to depression through the gut-brain axis, yet the underlying multi-level mechanisms remain unclear. This study aims to delineate the pathway from chronic restraint stress (CRS) to depressive-like behaviors, focusing on interactions among gut microbiota, their metabolites, and host transcriptional responses in the colon and hippocampus. METHODS: A CRS mice model was established and validated by behavioral tests. We performed 16S rRNA sequencing of gut microbiota, RNA-sequencing of colon and hippocampal tissues, and integrated these with assessments of intestinal histology, systemic and neuroinflammation, synaptic integrity, and levels of circulating neurotransmitters and microbial metabolites. Data were synthesized using bioinformatics and correlation network analyses. RESULTS: CRS induced significant depressive-like behaviors, hippocampal neuroinflammation, and synaptic damage. Additionally, it resulted in intestinal barrier damage, dysbiosis of the gut microbiota (e.g., an increase in Akkermansia/Dubosiella and a decrease in Ileibacterium), and a general decrease in fecal short-chain fatty acids (SCFAs). Transcriptomic analysis revealed tissue-specific disorders, with the circadian clock pathways in the colon (e.g. Nr1d1 and Nr1d2) being notably altered, while changes in the hippocampus were primarily concentrated on synaptic signaling. Correlation network analysis revealed significant correlations among microbiota alterations, reduced SCFAs, circadian clock gene dysregulation in the colon, systemic inflammation, and hippocampal pathological phenotypes. CONCLUSION: This study supports an integrated association framework linking gut microbiota imbalance, reduced SCFAs, colonic circadian alteration, and depressive-like behavior, and highlights a novel 'gut microbiota-SCFAs-colonic clock' axis associated with stress-related phenotypes. Disruption of this axis is correlated with systemic inflammation and alterations in the hippocampal synaptic gene network, providing a new target for the intervention of stress-related mental disorders.
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Gut microbiome, and immune cells mediated effect on depression: A two-step, two-sample Mendelian randomization analysis.
BACKGROUND: The gut microbiota (GM) plays an important role in the development of immune-related diseases, and the immune response is one of the pathomechanisms of depression (Dep); whether the effect of GM on Dep is mediated by immune cells (ImC) is unclear. OBJECTIVE: ImC may mediate the effect of GM on Dep. Our aim is to identify and quantify the role of immune characteristics as potential mediators. METHODS: Pooled statistics for GM (n = 7738) and ImC (n = 3757) were obtained from publicly available genome-wide association studies (GWAS), and for Dep (n = 47,696) from the Finnish database R10. We used a mediated Mendelian randomization (MR) study to investigate the causal relationship between GM and Dep and the mediating role of ImC between GM and Dep associations. RESULTS: The results showed that the genetically predicted GM was significantly correlated with both ImC as well as Dep. MR analysis identified five microbiomes that had significant causal effects on Dep (Methionine biosynthesis III, PWY-6737-Starch degradation V, Parasutterella excrementihominis, Parasutterella, and Lysine biosynthesis I). In addition, five of the 26 ImC trait significantly associated with GM were most closely associated with Dep (T cell %lymphocyte、CD28-CD127-CD25++CD8br AC、CD28-CD8br AC、CD27 receptor on peripheral blood plasma cells (CD27 on PB/PC) and CD11b receptor on mononuclear myeloid-derived suppressor cells (CD11b on Mo MDSC)). This mediated MR illustrates the causal role of methionine biosynthesis III on Dep (IVW: OR = 1.08, 95%CI [1.04,1.14], P = 0.001). And there was no strong evidence for a causal effect of depression on methionine biosynthesis III. In the B cell group, the proportion of CD27 on PB/PC mediated was 7.88 %(95%CI [-0.04,0.03]) of the total effect. This study further suggests that Dep patients should actively seek immunologic intervention therapy. CONCLUSION: This MR study found that GM may play a causal role in Dep by mediating ImC. Our findings will help to understand the pathogenic mechanism of GM in Dep and the risk of immune mediation.
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Leonurine Regulates Hippocampal Nerve Regeneration in Rats with Chronic and Unpredictable Mild Stress by Activating SHH/GLI Signaling Pathway and Restoring Gut Microbiota and Microbial Metabolic Homeostasis.
Depression is a highly prevalent and heterogeneous disorder that requires new strategies to overcome depression. In this study, we aimed to investigate whether leonurine modulated hippocampal nerve regeneration in chronic and unpredictable mild stress (CUMS) rats through the SHH/GLI signaling pathway and restoring gut microbiota and microbial metabolic homeostasis. The CUMS rat model was constructed and treated with leonurine. The body weight of rats was recorded, and a series of tests were performed. Western blot was utilized to measure the expression of BDNF and 5-HT in the hippocampus. Then the expression of SHH, GLI, PTCH, and SMO were measured by qRT-PCR and western blot. The colocalization of BrdU+DCX and BrdU+NeuN was evaluated by IF. 16S rDNA high-throughput sequencing was applied to detect the composition and distribution of gut microbiota. The differential metabolites were analyzed by untargeted metabolomics. The correlation between gut microbiota and microbial metabolites was analyzed by Pearson correlation coefficient. After CUMS modeling, the body weight of rats was decreased, and the expression of BDNF and 5-HT were decreased, while the body weight was recovered, and the expression of BDNF and 5-HT were increased after leonurine treatment. Leonurine reversed the reduction in the colocalization of BrdU+DCX and BrdU+NeuN and the reduction in the levels of SHH, GLI, PTCH, and SMO induced by CUMS modeling. Leonurine also restored gut microbiota and microbial metabolites homeostasis in CUMS rats. Furthermore, Prevotellaceae_Ga6A1_group was negatively correlated with 3-Oxocholic acid, nutriacholic acid, and cholic acid. Collectively, leonurine regulated hippocampal nerve regeneration in CUMS rats by activating the SHH/GLI signaling pathway and restoring gut microbiota and microbial metabolic homeostasis.
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The antidepressant potential of lactobacillus casei in the postpartum depression rat model mediated by the microbiota-gut-brain axis.
Lactobacillus casei, a kind of probiotic, was reported as antidepressant effects. However, little is known about the effect of Lactobacillus casei on postpartum depression (PPD). In this study, we investigated the effects of Lactobacillus casei in improving PPD and potential mechanisms. Four hours of daily maternal separation from postnatal day 2 to day 21 was performed to establish the PPD model in rats. From postnatal day 2 to day 28, rats were gavage-fed with an equal volume of normal saline, Lactobacillus casei (8 × 108 CFU/kg/day), or paroxetine (1.8 mg/kg/day), respectively. Rat behaviors were measured using the sucrose preference test, the elevated plus maze, the forced swim test, and the tail suspension test. Changes in gut microbiota were detected by real-time fluorescence quantitative PCR. Administration of Lactobacillus casei improved depressive-like behaviors, intestinal microflora, and oxidative stress in PPD model rats. Western Blot or HPLC assays showed that Lactobacillus casei intervention reversed the changes of brain-derived neurotrophic factor (BDNF), N-methyl-D-aspartic acid receptor 1 (NR1), ERK1/2, and monoamines in the brain of PPD rats. These results suggest that Lactobacillus casei could improve PPD through altering gut microbiota composition, brain monoamines and oxidative stress, which may be associated with the regulation of the BDNF-ERK1/2 pathway.
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Gut microbiota dysbiosis-mediated ceramides elevation contributes to corticosterone-induced depression by impairing mitochondrial function.
The role of gut microbiota (GM) dysbiosis in the pathogenesis of depression has received widespread attention, but the mechanism remains elusive. Corticosterone (CORT)-treated mice showed depression-like behaviors, reduced hippocampal neurogenesis, and altered composition of the GM. Fecal microbial transplantation from CORT-treated mice transferred depression-like phenotypes and their dominant GM to the recipients. Fecal metabolic profiling exposed remarkable increase of gut ceramides in CORT-treated and recipient mice. Oral gavage with Bifidobacterium pseudolongum and Lactobacillus reuteri could induce elevations of gut ceramides in mice. Ceramides-treated mice showed depressive-like phenotypes, significant downregulation of oxidative phosphorylation-associated genes, and hippocampal mitochondrial dysfunction. Our study demonstrated a link between chronic exposure to CORT and its impact on GM composition, which induces ceramides accumulation, ultimately leading to hippocampal mitochondrial dysfunction. This cascade of events plays a critical role in reducing adult hippocampal neurogenesis and is strongly associated with the development of depression-like behaviors.
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Long-term and trimester-specific effects of prenatal stress on the child gut microbiota.
OBJECTIVE: Stress is common among pregnant individuals and is associated with an altered gut microbiota composition in infants. It is unknown if these compositional changes persist into the preschool years when the gut microbiota reaches an adult-like composition. This study aimed to investigate if indicators of prenatal stress (i.e., psychological distress and stress-related physiology) are associated with children's gut microbiota composition and metabolites at 3-4 years of age. METHODS: Maternal-child pairs (n = 131) were from the Alberta Pregnancy Outcomes and Nutrition (APrON) cohort. Each trimester, psychological distress was measured as symptoms of anxiety (Symptom Checklist-90-R) and depressed mood (Edinburgh Postnatal Depression Scale), whereas salivary cortisol was quantified as a measure of stress-related physiology. Child stool samples were collected at 3-4 years to evaluate gut microbiota composition using 16S rRNA gene sequencing and fecal metabolome using liquid chromatography with tandem mass spectrometry (LC-MS/MS). Associations between prenatal distress and cortisol with the gut microbiota were determined using Pearson and Spearman correlations and corrected for multiple testing. Associations between prenatal distress and cortisol with the fecal metabolome were assessed using Metaboanalyst. RESULTS: Symptoms of depressed mood during the 2nd and 3rd trimesters and anxiety during the 2nd trimester of pregnancy were associated with increased alpha diversity of the child's gut microbiota. Cortisol levels during the 1st trimester were also associated with increased Faith PD diversity (r = 0.32), whereas cortisol levels during the 2nd trimester were associated with reduced Shannon diversity (r = -0.27). Depression scores during the 2nd and 3rd trimesters were associated with reductions in the relative abundances of Eggerthella, Parasutterella, and increases in Ruminococcaceae (rs = -0.28, rs = -0.32, rs = 0.32, respectively), as well as the fecal metabolome (e.g., branched-chain amino acid metabolism). Cortisol levels during the 2nd trimester correlated with 7 bacterial taxa, whereas 1st-trimester cortisol levels were associated with the child's fecal metabolome. CONCLUSIONS: Prenatal distress and cortisol were associated with both child gut microbiota composition and fecal metabolome at preschool age. Understanding these associations may allow for the identification of microbiota-targeted interventions to support child developmental outcomes affected by prenatal stress.
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Bidirectional relationship between gastrointestinal cancer and depression: The key is in the microbiota-gut-brain axis.
In this Editorial, we review the recent publication in the World Journal of Gastroenterology, which explores the complex relationship between depression and gastric cancer and offers perspectives. Key topics discussed include the microbiota-gut-brain axis, dysbiosis, and the influence of microbial metabolites in homeostasis. Additionally, we address toxic stress caused by hypothalamic-pituitary-adrenal axis dysregulation, psychological assessments, and future research directions. Our Editorial aims to expand the understanding of the bidirectional relationship between depression and gastrointestinal cancer.