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Characterization of gut microbiome in mice model of depression with divergent response to escitalopram treatment.
Depression is a common and heterogeneous mental disorder. Although several antidepressants are available to treat the patients with depression, the factors which could affect and predict the treatment response remain unclear. Here, we characterize the longitudinal changes of microbial composition and function during escitalopram treatment in chronic unpredictable mild stress (CUMS) mice model of depression based on 16 S rRNA sequencing and metabolomics. Consequently, we found that escitalopram (ESC) administration serves to increase the alpha-diversity of the gut microbiome in ESC treatment group. The microbial signatures between responder (R) and non-responder (NR) groups were significantly different. The R group was mainly characterized by increased relative abundances of genus Prevotellaceae_UCG-003, and depleted families Ruminococcaceae and Lactobacillaceae relative to NR group. Moreover, we identified 15 serum metabolites responsible for discriminating R and NR group. Those differential metabolites were mainly involved in phospholipid metabolism. Significantly, the bacterial OTUs belonging to family Lachnospiraceae, Helicobacteraceae, and Muribaculaceae formed strong co-occurring relationships with serum metabolites, indicating alternations of gut microbiome and metabolites as potential mediators in efficiency of ESC treatment. Together, our study demonstrated that the alterations of microbial compositions and metabolic functions might be relevant to the different response to ESC, which shed new light in uncovering the mechanisms of differences in efficacy of antidepressants.
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Edinburgh postpartum depression scores are associated with vaginal and gut microbiota in pregnancy.
BACKGROUND: Prenatal and postpartum depression may be influenced by the composition of host associated microbiomes. As such, the objective of this study was to elucidate the relationship between the human gut or vaginal microbiomes in pregnancy with prenatal or postpartum depression. METHODS: 140 female participants were recruited at their first prenatal visit and completed the Edinburgh Postnatal Depression Scale (EPDS) to screen for depression and anxiety, in addition the EPDS was completed one month postpartum. Vaginal and stool biospecimens were collected in the third trimester, analyzed using 16S rRNA gene sequencing, and assessed for alpha and beta diversity. Individual taxa differences and clustering using the k-medoids algorithm enabled community state type classification. RESULTS: Participants with higher postpartum EPDS scores had higher species richness and lower abundance of L. crispatus in the vaginal microbiota compared to those with lower EPDS scores. Participants with a higher prenatal EPDS score had lower species richness of the gut microbiome. Participants with a vaginal community state type dominated by L. iners had the highest mean prenatal EPDS scores, whereas postpartum EPDS scores were similar regardless of prenatal vaginal state type. LIMITATIONS: Our small sample size and participant's self-report bias limits generalizability of results. CONCLUSIONS: Depression in the prenatal and postpartum period is associated with the composition and diversity of the gut and vaginal microbiomes in the third trimester of pregnancy. These results provide a foundational understanding of the microbial relationships between maternal health and depression for identifying potential therapeutic treatments.
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How stress, discrimination, acculturation and the gut microbiome affect depression, anxiety and sleep among Chinese and Korean immigrants in the USA: a cross-sectional pilot study protocol.
INTRODUCTION: Although a considerable proportion of Asians in the USA experience depression, anxiety and poor sleep, these health issues have been underestimated due to the model minority myth about Asians, the stigma associated with mental illness, lower rates of treatment seeking and a shortage of culturally tailored mental health services. Indeed, despite emerging evidence of links between psychosocial risk factors, the gut microbiome and depression, anxiety and sleep quality, very few studies have examined how these factors are related in Chinese and Korean immigrants in the USA. The purpose of this pilot study was to address this issue by (a) testing the usability and feasibility of the study's multilingual survey measures and biospecimen collection procedure among Chinese and Korean immigrants in the USA and (b) examining how stress, discrimination, acculturation and the gut microbiome are associated with depression, anxiety and sleep quality in this population. METHOD AND ANALYSIS: This is a cross-sectional pilot study among first and second generations of adult Chinese and Korean immigrants in the greater Atlanta area (Georgia, USA). We collected (a) gut microbiome samples and (b) data on psychosocial risk factors, depression, anxiety and sleep disturbance using validated, online surveys in English, Chinese and Korean. We aim to recruit 60 participants (30 Chinese, 30 Korean). We will profile participants' gut microbiome using 16S rRNA V3-V4 sequencing data, which will be analysed by QIIME 2. Associations of the gut microbiome and psychosocial factors with depression, anxiety and sleep disturbance will be analysed using descriptive and inferential statistics, including linear regression. ETHICS AND DISSEMINATION: This study has been approved by the Institutional Review Board at Emory University (IRB ID: STUDY00000935). Results will be made available to Chinese and Korean community members, the funder and other researchers and the broader scientific community.
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BDNF/CREB signaling pathway contribution in depression pathogenesis: A survey on the non-pharmacological therapeutic opportunities for gut microbiota dysbiosis.
Emerging evidence supports the gut microbiota and the brain communication in general health. This axis may affect behavior through modulating neurotransmission, and thereby involve in the pathogenesis and/or progression of different neuropsychiatric disorders such as depression. Brain-derived neurotrophic factor and cAMP response element-binding protein known as CREB/BDNF pathway plays have critical functions in the pathogenesis of depression as the same of mechanisms related to antidepressants. However, the putative causal significance of the CREB/BDNF signaling cascade in the gut-brain axis in depression remains unknown. Also interventions such as probiotics supplementation and exercise can influence microbiome also improve bidirectional communication of gut and brain. In this review we aim to explain the BDNF/CREB signaling pathway and gut microbiota dysfunction and then evaluate the potential role of probiotics, prebiotics, and exercise as a therapeutic target in the gut microbiota dysfunction induced depression. The current narrative review will specifically focus on the impact of exercise and diet on the intestinal microbiota component, as well as the effect that these therapies may have on the microbiota to alleviate depressive symptoms. Finally, we look at how BDNF/CREB signaling pathway may exert distinct effects on depression and gut microbiota dysfunction.
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Gut-derived IL-17A via STAT3/RORγt signaling underlies sleep disruption-induced depression: Targeting effects of Schisandrin B therapy.
BACKGROUND: Circadian rhythm disruption and chronic sleep deprivation are increasingly recognized as key contributors to depression, largely through gut-brain axis dysregulation and neuroinflammatory activation. IL-17A, a pro-inflammatory cytokine primarily derived from intestinal Th17 cells, has emerged as a pivotal mediator linking gut immune imbalance to central nervous system dysfunction. PURPOSE: This study aimed to elucidate the gut-derived IL-17A-STAT3/RORγt signaling mechanism underlying sleep-deprivation-induced depression and to determine whether Schisandrin B, a lignan from Schisandra chinensis, can alleviate depressive phenotypes by restoring gut-brain axis homeostasis. METHODS: Clinical analyses of plasma cytokines and metabolites were integrated with a mouse model of sleep-deprivation-induced depression. Behavioral tests, resting-state fMRI, gut microbiota 16S rDNA sequencing, Western blotting, ELISA, and network pharmacology with molecular docking were employed to comprehensively investigate neuroimmune, microbial, and neurofunctional alterations. RESULTS: Patients with circadian rhythm disorder-related depression exhibited elevated IL-17A and systemic inflammatory cytokines, accompanied by metabolic dysregulation. Sleep-deprived mice showed depressive-like behaviors, intestinal barrier disruption, Th17/IL-17A pathway activation, and abnormal RS-fMRI activity in mood-regulating brain regions. Schisandrin B treatment markedly reversed these changes-restoring gut microbial balance, enhancing barrier integrity, suppressing IL-17A-driven inflammation, and normalizing neural function. Mechanistically, Schisandrin B inhibited STAT3 phosphorylation and RORγt expression, while targeting MAPK1 and GSK3β as key regulatory nodes. CONCLUSION: This study identifies gut-derived IL-17A-STAT3/RORγt signaling as a mechanistic bridge between sleep deprivation and neuroinflammation, providing direct evidence for the immunological basis of circadian rhythm-related depression. By integrating multi-omics and neuroimaging validation, we demonstrate for the first time that Schisandrin B exerts antidepressant-like effects via coordinated modulation of the gut-brain-immune network. These findings highlight Schisandrin B as a promising natural immunomodulatory candidate for the treatment of mood disorders associated with disrupted circadian rhythms.
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Changes in gut viral and bacterial species correlate with altered 1,2-diacylglyceride levels and structure in the prefrontal cortex in a depression-like non-human primate model.
Major depressive disorder (MDD) is a debilitating mental disease, but its underlying molecular mechanisms remain obscure. Our previously established model of naturally occurring depression-like (DL) behaviors in Macaca fascicularis, which is characterized by microbiota-gut-brain (MGB) axis disturbances, can be used to interrogate how a disturbed gut ecosystem may impact the molecular pathology of MDD. Here, gut metagenomics were used to characterize how gut virus and bacterial species, and associated metabolites, change in depression-like monkey model. We identified a panel of 33 gut virus and 14 bacterial species that could discriminate the depression-like from control macaques. In addition, using lipidomic analyses of central and peripheral samples obtained from these animals, we found that the DL macaque were characterized by alterations in the relative abundance, carbon-chain length, and unsaturation degree of 1,2-diacylglyceride (DG) in the prefrontal cortex (PFC), in a brain region-specific manner. In addition, lipid-reaction analysis identified more active and inactive lipid pathways in PFC than in amygdala or hippocampus, with DG being a key nodal player in these lipid pathways. Significantly, co-occurrence network analysis showed that the DG levels may be relevant to the onset of negative emotions behaviors in PFC. Together our findings suggest that altered DG levels and structure in the PFC are hallmarks of the DL macaque, thus providing a new framework for understanding the gut microbiome's role in depression.
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Lacticaseibacillus paracasei NK112 mitigates Escherichia coli-induced depression and cognitive impairment in mice by regulating IL-6 expression and gut microbiota.
The gut microbiota communicates with the brain through microbiota-gut-brain (MGB) and hypothalamus-pituitary-adrenal (HPA) axes and other pathways. Excessive expression of interleukin (IL)-6 is closely associated with the occurrence of the psychiatric disorders depression and dementia. Therefore, to understand whether IL-6 expression-suppressing probiotics could alleviate psychiatric disorders, we isolated IL-6 expression-inhibiting Lacticaseibacillus paracasei (formerly Lactobacillus paracasei) NK112 from the human faecal bacteria strain collection (Neurobiota Research Center, Seoul, Korea) and examined its therapeutic effect for the depression and cognitive impairment in mice. C57 BL/6J mice with depression and cognitive impairment were prepared by exposure to Escherichia coli K1. Oral gavage of NK112 significantly alleviated K1-induced anxious, depressive, and memory-impaired behaviours in the elevated plus maze, tail-suspension and Y-maze tasks, IL-1β, IL-6, and tumour necrosis factor (TNF)-α expression, and nuclear factor kappa beta (NF-κB) activation in the hippocampus, while K1-suppressed brain-derived neurotrophic factor (BDNF) expression increased. Treatment with NK112 also improved K1-induced myeloperoxidase activity, IL-6 and TNF-α expression, and NF-κB activation in the colon and reduced K1-induced Proteobacteria population in the gut microbiota. Heat-killed NK112 and its lysate supernatant, and precipitate fractions also improved anxiety/depression, cognitive impairment, and colitis in mice. In conclusion, NK112, even if heat-killed or lysed, alleviated K1 stress-induced colitis, anxiety/depression, and cognitive impairment by suppressing IL-6, TNF-α, and BDNF expression through the regulation of gut microbiota and NF-κB activation.
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Gegen Qinlian decoction alleviates depression-like behavior by modulating the gut microenvironment in CUMS rats.
BACKGROUND: Gegen Qinlian Decoction (GQD) is a classical traditional Chinese medicine (TCM) formula primarily utilized for treating gut disorders. GQD showed therapeutic effects on several diseases in clinical and animal studies by targeting gut microbes. Our recent studies also found that GQD efficiently alleviated anxiety in methamphetamine-withdrawn mice via regulating gut microbiome and metabolism. Given that various studies have indicated the link between the gut microbiome and the development of depression, here we endeavor to explore whether GQD can manage depression disorders by targeting the gut microbiome. METHODS AND MATERIALS: The depression-like model was induced in rats through chronic unpredictable mild stress (CUMS) and the depression levels were determined using the sucrose preference test (SPT). To address the depression-like behavior in rats, oral administration of GQD was employed. The colon microbiome and metabolite patterns were determined by 16s rRNA sequencing and untargeted metabolomics, respectively. RESULTS: We found 6 weeks of CUMS can induce depression-like behavior in rats and 4 weeks of GQD treatment can significantly alleviate the depression-like behavior. GQD treatment can also ameliorate the histological lesions in the colon of CUMS rats. Then, CUMS increased the abundance of gut microbes, while GQD treatment can restore it to a lower level. We further discovered that the abundances of 19 bacteria at the genus level were changed with CUMS treatment, among which the abundances of Ruminococcus, Lachnoclostridium, Pygmaiobacter, Bacteroides, Pseudomonas, and Pseudomonas Family_XIII_AD3011_group were stored by GQD treatment. Besides, we identified the levels of 36 colon metabolites were changed with CUMS treatment, among which the levels of Fasciculic acid B, Spermine, Fludrocortisone acetate, alpha-Ketoglutaric acid, 2-Oxoglutaric acid, N'-(benzoyloxy)-2-(2,2-dichlorocyclopropyl) ethanimidamide, N6-Succinyl Adenosine Oleanolic acid, KQH, Ergosta-5,7,9(11),22-Tetraen-3-beta-Ol, Gentisic acid, 4-Hydroxyretinoic Acid, FAHFA (3:0/16:0), Leucine-enkephalin and N-lactoyl-phenylalanine can be restored by GQD treatment. CONCLUSION: Our findings provide evidence supporting the therapeutic efficacy of GQD in alleviating depression-like behavior in CUMS rats, potentially being targeted on colon bacteria (especially the abundance of Ruminococcus and Bacteroides) and metabolites (especially the level of Oleanolic acid).
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Bifidobacterium with the role of 5-hydroxytryptophan synthesis regulation alleviates the symptom of depression and related microbiota dysbiosis.
Depression disorder is rapidly advancing worldwide, and therapeutic strategy through gut-brain axis has been proven to be effective in the treatment. Here we studied the effect of lactic acid bacteria (LAB) treatment on depression. C57BL/6J mice were administered with LAB during a 5-week chronic unpredictable mild stress. Bifidobacterium longum subsp. infantis E41 and Bifidobacterium breve M2CF22M7, which improved the expression of Tph1 and secretion of 5-hydroxytryptophan (5-HTP) in RIN14B cells, significantly reduced depressive behaviors of mice in the forced swim test, sucrose preference test and step-down test, as well as increased the level of 5-hydroxytryptamine and brain-derived neurotrophic factor concentration in brain. Besides, M2CF22M7 reduced the serum corticosterone level. E41 increased cecal butyrate level, which significantly and positively correlated with some depression-related indexes. Using 16S rRNA-amplicon sequencing of faces, E41 and M2CF22M7 were found to improve the chronic-stress-induced microbial dysbiosis. They also normalized the host's pathways involving metabolism and gene information processing. These results indicate that Bifidobacterium E41 and M2CF22M7 have an antidepressant effect in mice partly in a 5-HTP dependent and microbiota-regulating manner. Nurturing the gut microbiota with these strains may become an emerging therapeutic way for mood disorder.
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Comparative transcriptional analyses of the striatum in the chronic social defeat stress model in C57BL/6J male mice and the gut microbiota-dysbiosis model in Kumming mice.
Depression is a complex disorder with multiple contributing factors, and chronic stress has previously been recognized as a major causative factor, while gut microbes have also been found to be involved in depression recently. However, gene expression in depression models with different etiologies is unclear. Here, we compared the transcriptomes of the striatum in chronic social defeat stress (CSDS) model of C57BL/6J male mice and fecal microbiota transplant (FMT) model of Kumming male mice. We found that the proportion of shared differentially expressed genes (DEGs) between the two models was only 24 %. The specific DEGs of FMT model were enriched in immune and inflammatory, and are associated with changes in vascular and ciliated ependymal cells. The specific DEGs of CSDS model were enriched in neuron and synapse. The results of network analysis suggested the expression patterns and biological function of depressive-like behaviors-related modules in the two models are different. Further, the alternative splicing events of CSDS are more than FMT. Our results suggested models of depression induced by different etiologies differ significantly in gene expression and biological function. Our study also suggested us to pay attention to the characteristics of models of depression of different etiologies and provided a more comprehensive understanding of the heterogeneity of depression.