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Exploration of microbiota targets for major depressive disorder and mood related traits.
Growing evidence suggests the link between gut microbiota and mood regulation. The current study aimed to identify microbiota targets for major depressive disorder (MDD) and mood-related traits in Taiwanese samples, while taking into account the influence of dietary patterns. We recruited 36 MDD patients and 37 healthy controls for 16S rRNA gene sequencing. We assessed nutrient content using food frequency questionnaire, and mood related phenotypes, including depressive severity, anxiety, and perceived stress. Analysis of composition of microbiomes (ANCOM) models were performed to evaluate microbiota compositions between patients and controls, while adjusted for fat intake% and sequencing platforms. We found 23 taxa (4 phyla, 7 families and 12 genera) to be associated with depression and beta diversity was differed between groups. Phylum Actinobacteria and Firmicutes were overrepresented in MDD patients. At genus level, Bifidobacterium (7%) and Blautia (8%) had relatively high abundance among MDD patients, while Prevotella (16%) had high abundance in controls. Holdemania exhibited moderate correlation with anxiety (r = 0.65) and perceived stress level (r = 0.49) mainly in MDD patients but not controls. Pathway analyses revealed that pentose phosphate and starch and sucrose metabolism processes were important pathways for depression via microbiota functions. In conclusion, our results revealed microbiota targets for depression that are independent of fat intake. It is worthwhile to conduct further studies to replicate the current findings and to integrate with biochemistry and metabolomics data to better understand the functions of identified targets.
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Comparative metaproteomics analysis shows altered fecal microbiota signatures in patients with major depressive disorder.
Major depressive disorder (MDD) is a highly prevalent and debilitating mental illness, which is associated with disorder of gut microbiota. However, few studies focusing on detection of the signatures of bacteria in feces of MDD patients using proteomics approach have been carried out. Here, a comparative metaproteomics analysis on the basis of an isobaric tag for relative and absolute quantification coupled with tandem mass spectrometry was carried out to explore the signature of gut microbiota in patients with MDD. Ten patients (age: 18-56 years, five women) who had MDD and a score over 20 on the Hamilton's Depression Scale and 10 healthy controls (age: 24-65 years, five women) group matched for sex, age, and BMI were enrolled. As a result, 279 significantly differentiated bacterial proteins (P<0.05) were detected and used for further bioinformatic analysis. According to phylogenetic analysis, statistically significant differences were observed for four phyla: Bacteroidetes, Proteobacteria, Firmicutes, Actinobacteria (P<0.05, for each). Abundances of 16 bacterial families were significantly different between the MDD and healthy controls (P<0.05). Furthermore, Cluster of Orthologous Groups analysis and Kyoto Encyclopedia of Genes and Genomes pathway analysis showed that disordered metabolic pathways of bacterial proteins were mainly involved in glucose metabolism and amino acid metabolism. In conclusion, fecal microbiota signatures were altered significantly in MDD patients. Our findings provide a novel insight into the potential connection between gut microbiota and depression.
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Psychophysiological Effects of Lactobacillus plantarum PS128 in Patients with Major Depressive Disorder: A Preliminary 8-Week Open Trial.
Recent studies have suggested that gut-brain axis may be one of the mechanisms of major depression disorder (MDD). The current study aimed to investigate the effects of Lactobacillus plantarum PS128 (PS128) on psychophysiology in patients with MDD. We recruited 11 patients with MDD and gave them PS128 for 8 weeks. We compared depression symptoms, serum markers of inflammation and gut permeability, and gut microbiota before and after 8-week intervention and also explored the correlations among symptoms, biomarkers, and gut microbiota. After 8-week PS128 intervention, scores of Hamilton Depression Rating Scale-17 and Depression and Somatic symptoms Scale significantly decreased. Serum levels of high sensitivity c-reactive protein, interluekin-6, and tumor necrosis factor-α, zonulin and intestinal fatty acid binding protein, and the composition of gut microbiota did not significantly change after 8-week PS128 intervention. However, we found changes of some genera were correlated with changes of symptoms and biomarkers. In conclusion, this is an open trial with small sample size and has several limitations. The results need to be verified by randomized, double-blind, placebo-controlled trial with larger sample size.
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Weight Gain During SSRI Therapy: The Potential Role of the Gut Microbiota-A Narrative Review and Mechanistic Hypothesis.
Introduction: Selective serotonin reuptake inhibitors (SSRIs) remain the first-line pharmacological treatment for depressive disorders. However, long-term treatment is often accompanied by weight gain, which negatively impacts medication adherence and cardiometabolic health. Emerging evidence suggests that, in addition to their effects on the central nervous system (CNS), SSRIs may alter the composition and metabolic activity of the gut microbiome, potentially contributing to metabolic disorders. However, the mechanisms linking SSRI-induced microbial changes to weight regulation remain poorly understood. Methods: This narrative review summarizes the current evidence regarding the interactions between SSRIs, the gut microbiome, host metabolism, and weight regulation. Experimental, translational, and clinical studies were critically assessed, with particular emphasis on recent systematic reviews, meta-analyses, randomized controlled trials, and mechanistic studies. A conceptual mechanistic framework was developed based on the available evidence. Results: Experimental and clinical studies indicate that SSRIs can modify both the taxonomic composition and functional activity of the gut microbiota. These changes may influence the production of microbiota-derived metabolites, including short-chain fatty acids, bile acids, and tryptophan metabolites, thereby influencing gut barrier integrity, low-grade inflammation, gut hormone secretion, appetite regulation, and energy homeostasis. Current evidence also suggests that dietary interventions-including increased dietary fiber intake, adherence to a Mediterranean diet, and microbiota-targeted strategies using prebiotics, probiotics, synbiotics, and postbiotics-can beneficially modulate these pathways. However, no randomized, controlled trials have specifically assessed whether such interventions prevent SSRI-associated weight gain. Conclusions: Taken together, the available evidence raises the possibility that gut microbiota alterations may contribute to SSRI-associated weight gain, although this hypothesis has not yet been directly tested in studies evaluating the complete mechanistic pathway.
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Synbiotic HQP08 Supplementation for Hair Loss and Depressive Symptoms: An Open-Label Pilot Study of Clinical Outcomes and Gut Microbiome Changes.
Background: Gut microbiota dysregulation has been implicated in hair loss via the gut-skin axis, but human interventional data are limited. We previously showed that Bifidobacterium longum HK003 reverses alopecia-like phenotypes in mice. Methods: We conducted an open-label, single-arm pilot study to evaluate an HK003-containing synbiotic (HQP08) in 32 adults with self-reported hair loss over 8 weeks. The primary endpoint was the proportion of participants reporting improvement on the Patient Global Impression of Change (PGI-C) scale at week 8. Secondary outcomes included changes in hair loss severity, 60 s hair count, depressive symptoms (PHQ-9), safety, and gut microbiome composition (Chinese Clinical Trial Registry ChiCTR2500112698). Results: At week 8, 62.5% (20/32) of participants reported PGI-C improvement. Significant reductions were observed in hair loss severity (p = 0.0008), 60 s hair count (p = 0.0048), and PHQ-9 scores (p = 0.002). Younger age was associated with PGI-C response (OR per year 0.86, 95% CI: 0.73-0.98, p = 0.037). Metagenomic analysis identified engraftment of B. longum HK003-like profiles in a subset of participants at week 12. Changes in microbial pathways related to thiamine metabolism, vitamin B12 salvage, and lipopolysaccharide biosynthesis were associated with ΔPHQ-9 (FDR-adjusted p < 0.05), but not with hair-related endpoints. No serious adverse events occurred. Conclusions: This first-in-human pilot study suggests that HQP08 was well tolerated and was associated with within-participant changes in hair-loss measurements and PHQ-9 scores. Randomized controlled trials are warranted to confirm efficacy and further elucidate mechanisms within the gut-brain-skin axis.
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Long-lasting Depressive Behavior of Adolescent Chronically Stressed Mice is Mediated by Gut Microbiota Dysbiosis.
Depression is one of the most common mental disorders worldwide, and its prevalence sharply rises during adolescence. Adolescence is a particularly sensitive period to the effects of environmental stressors, which can cause persistent depressive behavior extending into adulthood. However, the studies assessing if changes in gut microbiota could be one of the mediators of long-term effects of adolescent stress are scarce. In the present study, we examined enduring effects of adolescent chronic unpredictable stress (CUS) on mice behavior along with alterations in their gut microbiome, by using 16 s rRNA gene sequencing and fecal microbiota transplantation (FMT). CUS mice, as well as naïve mice receiving FMT from stressed animals, showed long-lasting anxiety and depressive-like behavior extending into adulthood. The microbiota dysbiosis in adolescence was characterized by higher abundance of Alloprevotella and lower abundance of Paraprevotella, Parasutterella, Parabacteroides, and undefined genus Rikenellaceae_RC9_gut_group. On the contrary, microbiota dysbiosis in adulthood was characterized by higher abundance of Bacteroides, Enterorhabdus, Marvinbriantia, and Parabacteroides and lower abundance of Akkermansia, Odoribacter, and Rikenella. In particular, depressive-like behavior in adolescence was negatively correlated with Paraprevotella, while depressive-like behavior in adulthood was negatively correlated with Rikenella abundance, in both CUS and FMT mice. Therefore, the transfer of microbiota from mice stressed in adolescence is able to induce long-lasting depressive-like behavior in naïve mice, clearly showing the importance of gut microbiota dysbiosis in adolescence in shaping enduring depressive behavior. Moreover, our results indicate that changes in specific but different bacteria are related to depressive behavior in adolescence and in adulthood.
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Metabolite identification in fecal microbiota transplantation mouse livers and combined proteomics with chronic unpredictive mild stress mouse livers.
Major depressive disorder (MDD) is a common mood disorder. Gut microbiota may be involved in the pathogenesis of depression via the microbe-gut-brain axis. Liver is vulnerable to exposure of bacterial products translocated from the gut via the portal vein and may be involved in the axis. In this study, germ-free mice underwent fecal microbiota transplantation from MDD patients and healthy controls. Behavioral tests verified the depression model. Metabolomics using gas chromatography-mass spectrometry, nuclear magnetic resonance, and liquid chromatography-mass spectrometry determined the influence of microbes on liver metabolism. With multivariate statistical analysis, 191 metabolites were distinguishable in MDD mice from control (CON) mice. Compared with CON mice, MDD mice showed lower levels for 106 metabolites and higher levels for 85 metabolites. These metabolites are associated with lipid and energy metabolism and oxidative stress. Combined analyses of significantly changed proteins in livers from another depression model induced by chronic unpredictive mild stress returned a high score for the Lipid Metabolism, Free Radical Scavenging, and Molecule Transports network, and canonical pathways were involved in energy metabolism and tryptophan degradation. The two mouse models of depression suggest that changes in liver metabolism might be involved in the pathogenesis of MDD. Conjoint analyses of fecal, serum, liver, and hippocampal metabolites from fecal microbiota transplantation mice suggested that aminoacyl-tRNA biosynthesis significantly changed and fecal metabolites showed a close relationship with the liver. These findings may help determine the biological mechanisms of depression and provide evidence about "depression microbes" impacting on liver metabolism.
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Komagataella pastoris KM71H Mitigates Depressive-Like Phenotype, Preserving Intestinal Barrier Integrity and Modulating the Gut Microbiota in Mice.
The role of intestinal microbiota in the genesis of mental health has received considerable attention in recent years, given that probiotics are considered promising therapeutic agents against major depressive disorder. Komagataella pastoris KM71H is a yeast with probiotic properties and antidepressant-like effects in animal models of depression. Hence, we evaluated the antidepressant-like effects of K. pastoris KM71H in a model of antibiotic-induced intestinal dysbiosis in male Swiss mice. The mice received clindamycin (200 μg, intraperitoneal) and, after 24 h, were treated with K. pastoris KM71H at a dose of 8 log CFU/animal by intragastric administration (ig) or PBS (vehicle, ig) for 14 consecutive days. Afterward, the animals were subjected to behavioral tests and biochemical analyses. Our results showed that K. pastoris KM71H administration decreased the immobility time in the tail suspension test and increased grooming activity duration in the splash test in antibiotic-treated mice, thereby characterizing its antidepressant-like effect. We observed that these effects of K. pastoris KM71H were accompanied by the modulation of the intestinal microbiota, preservation of intestinal barrier integrity, and restoration of the mRNA levels of occludin, zonula occludens-1, zonula occludens-2, and toll-like receptor-4 in the small intestine, and interleukin-1β in the hippocampi of mice. Our findings provide solid evidence to support the development of K. pastoris KM71H as a new probiotic with antidepressant-like effects.
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Role of Actinobacteria and Coriobacteriia in the antidepressant effects of ketamine in an inflammation model of depression.
Ketamine, an N-methyl-d-aspartic acid receptor (NMDAR) antagonist, elicits rapid-acting and sustained antidepressant effects in treatment-resistant depressed patients. Accumulating evidence suggests that gut microbiota via the gut-brain axis play a role in the pathogenesis of depression, thereby contributing to the antidepressant actions of certain compounds. Here we investigated the role of gut microbiota in the antidepressant effects of ketamine in lipopolysaccharide (LPS)-induced inflammation model of depression. Ketamine (10 mg/kg) significantly attenuated the increased immobility time in forced swimming test (FST), which was associated with the improvements in α-diversity, consisting of Shannon, Simpson and Chao 1 indices. In addition to α-diversity, β-diversity, such as principal coordinates analysis (PCoA), and linear discriminant analysis (LDA) coupled with effect size measurements (LEfSe), showed a differential profile after ketamine treatment. Furthermore, a total of 30 bacteria were significantly altered in the LPS + saline treated mice and LPS + ketamine treated mice. Interestingly, two bacteria, including the phylum Actinobacteria and the class Coriobacteriia were significantly correlated with the immobility time of FST. Importantly, the receiver operating characteristic (ROC) curves demonstrated that the phylum Actinobacteria and the class Coriobacteriia were potential biomarker for the antidepressant effects of ketamine in an inflammation model. These findings suggest that antidepressant effects of ketamine might be related to the regulation of abnormal composition of gut microbiota, and that the phylum Actinobacteria and the class Coriobacteriia might be potential biomarkers for ketamine's antidepressant efficacy.
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A step ahead: Exploring the gut microbiota in inpatients with bipolar disorder during a depressive episode.
OBJECTIVES: There is evidence that the gut microbiota plays a major role in the pathogenesis of diseases of the central nervous system through the gut-brain axis. The aim of the present study was to analyze gut microbiota composition in bipolar disorder (BD) and its relation to inflammation, serum lipids, oxidative stress, tryptophan (TRP)/kynurenine (KYN) levels, anthropometric measurements and parameters of metabolic syndrome. Further, microbial community differences of individuals with BD compared with healthy controls (HC) were explored. METHODS: In this cross-sectional study, we performed 16S rRNA gene sequencing of stool samples from 32 BD individuals and 10 HC. Laboratory parameters included inflammatory markers, serum lipids, KYN, oxidative stress and anthropometric measures. Microbial community analysis and correlation to clinical parameters was performed with QIIME, differential abundance analysis of taxa encompassed linear discriminant analysis effect size (LEfSe). RESULTS: We found a negative correlation between microbial alpha-diversity and illness duration in BD (R = -0.408, P = 0.021). Furthermore, we identified bacterial clades associated with inflammatory status, serum lipids, TRP, depressive symptoms, oxidative stress, anthropometrics and metabolic syndrome in individuals with BD. LEfSe identified the phylum Actinobacteria (LDA= 4.82, P = 0.007) and the class Coriobacteria (LDA= 4.75, P = 0.010) as significantly more abundant in BD when compared with HC, and Ruminococcaceae (LDA= 4.59, P = 0.018) and Faecalibacterium (LDA= 4.09, P = 0.039) as more abundant in HC when compared with BD. CONCLUSIONS: The present findings suggest that causes and/or consequences of BD may also lie outside the brain. Exploratory research of the gut microbiota in affective disorders like BD may identify previously unknown underlying causes, and offer new research and therapeutic approaches to mood disorders.