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Bacopaside I alleviates depressive-like behaviors by modulating the gut microbiome and host metabolism in CUMS-induced mice.
Bacopaside I (BSI) is a natural compound that is difficult to absorb orally but has been shown to have antidepressant effects. The microbiota-gut-brain axis is involved in the development of depression through the peripheral nervous system, endocrine system, and immune system and may be a key factor in the effect of BSI. Therefore, this study aimed to investigate the potential mechanism of BSI in the treatment of depression via the microbiota-gut-brain axis and to validate it in a fecal microbiota transplantation model. The antidepressant effect of BSI was established in CUMS-induced mice using behavioral tests and measurement of changes in hypothalamicpituitaryadrenal (HPA) axis-related hormones. The improvement of stress-induced gut-brain axis damage by BSI was observed by histopathological sections and enzyme-linked immunosorbent assay (ELISA). 16 S rDNA sequencing analysis indicated that BSI could modulate the abundance of gut microbiota and increase the abundance of probiotic bacteria. We also observed an increase in short-chain fatty acids, particularly acetic acid. In addition, BSI could modulate the disruption of lipid metabolism induced by CUMS. Fecal microbiota transplantation further confirmed that disruption of the microbiota-gut-brain axis is closely associated with the development of depression, and that the microbiota regulated by BSI exerts a partial antidepressant effect. In conclusion, BSI exerts antidepressant effects by remodeling gut microbiota, specifically through the Lactobacillus and Streptococcus-acetic acid-neurotrophin signaling pathways. Furthermore, BSI can repair damage to the gut-brain axis, regulate HPA axis dysfunction, and maintain immune homeostasis.
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A gut (microbiome) feeling about the brain.
PURPOSE OF REVIEW: There is an increasing realization that the microorganisms which reside within our gut form part of a complex multidirectional communication network with the brain known as the microbiome-gut-brain axis. In this review, we focus on recent findings which support a role for this axis in modulating neurodevelopment and behavior. RECENT FINDINGS: A growing body of research is uncovering that under homeostatic conditions and in response to internal and external stressors, the bacterial commensals of our gut can signal to the brain through a variety of mechanisms to influence processes such neurotransmission, neurogenesis, microglia activation, and modulate behavior. Moreover, the mechanisms underlying the ability of stress to modulate the microbiota and also for microbiota to change the set point for stress sensitivity are being unraveled. Dysregulation of the gut microbiota composition has been identified in a number of psychiatric disorders, including depression. This has led to the concept of bacteria that have a beneficial effect upon behavior and mood (psychobiotics) being proposed for potential therapeutic interventions. SUMMARY: Understanding the mechanisms by which the bacterial commensals of our gut are involved in brain function may lead to the development of novel microbiome-based therapies for these mood and behavioral disorders.
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Decreased gut microbiome-derived indole-3-propionic acid mediates the exacerbation of myocardial ischemia/reperfusion injury following depression via the brain-gut-heart axis.
Despite the increasing recognition of the interplay between depression and cardiovascular disease (CVD), the precise mechanisms by which depression contributes to the pathogenesis of cardiovascular disease remain inadequately understood. The involvement of gut microbiota and their metabolites to health and disease susceptibility has been gaining increasing attention. In this study, it was found that depression exacerbated cardiac injury, impaired cardiac function (EF%: P < 0.01; FS%: P < 0.05), hindered long-term survival (P < 0.01), and intensified adverse cardiac remodeling (WGA: P < 0.01; MASSON: P < 0.0001) after myocardial ischemia/reperfusion (MI/R) in mice. Then we found that mice receiving microbiota transplants from chronic social defeat stress (CSDS) mice exhibited worse cardiac function (EF%: P < 0.01; FS%: P < 0.01) than those receiving microbiota transplants from non-CSDS mice after MI/R injury. Moreover, impaired tryptophan metabolism due to alterations in gut microbiota composition and structure was observed in the CSDS mice. Mechanistically, we analyzed the metabolomics of fecal and serum samples from CSDS mice and identified indole-3-propionic acid (IPA) as a protective agent for cardiomyocytes against ferroptosis after MI/R via NRF2/System xc-/GPX4 axis, played a role in mediating the detrimental influence of depression on MI/R. Our findings provide new insights into the role of the gut microbiota and IPA in depression and CVD, forming the basis of intervention strategies aimed at mitigating the deterioration of cardiac function following MI/R in patients experiencing depression.
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Unraveling the gut-brain connection: The association of microbiota-linked structural brain biomarkers with behavior and mental health.
AIM: The gut microbiota can influence human behavior. However, due to the massive multiple-testing problem, research into the relationship between microbiome ecosystems and the human brain faces drawbacks. This problem arises when attempting to correlate thousands of gut bacteria with thousands of brain voxels. METHODS: We performed brain magnetic resonance imaging (MRI) scans on 133 participants and applied machine-learning algorithms (Ridge regressions) combined with permutation tests. Using this approach, we were able to correlate specific gut bacterial families with brain MRI signals, circumventing the difficulties of massive multiple testing while considering sex, age, and body mass index as confounding factors. RESULTS: The relative abundance (RA) of the Selenomonadaceae, Clostridiaceae, and Veillonellaceae families in the gut was associated with altered cerebellar, visual, and frontal T2-mapping and diffusion tensor imaging measures. Conversely, decreased relative abundance of the Eubacteriaceae family was also linked to T2-mapping values in the cerebellum. Significantly, the brain regions associated with the gut microbiome were also correlated with depressive symptoms and attentional deficits. CONCLUSIONS: Our analytical strategy offers a promising approach for identifying potential brain biomarkers influenced by gut microbiota. By gathering a deeper understanding of the microbiota-brain connection, we can gain insights into the underlying mechanisms and potentially develop targeted interventions to mitigate the detrimental effects of dysbiosis on brain function and mental health.
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Thyroid Dysfunction as a Component of an Immuno-Metabolic Depression-A Possible Role of Gut Microbiota and a Rationale for Future Studies.
Depression is one of the most prevalent psychiatric disorders worldwide, with a steadily increasing incidence and complex, multifactorial pathophysiology. Beyond classical neurochemical mechanisms, growing evidence points to the role of systemic low-grade inflammation and immuno-metabolic disturbances in its development. Gut microbiota dysbiosis has emerged as a key factor linking metabolic, immune, and neuroendocrine pathways, potentially exacerbating neuroinflammation and contributing to the onset and progression of depressive symptoms. Immune activation, which is a result of gut dysbiosis, may play a crucial role in the pathogenesis of immuno-metabolic depression. Thyroid dysfunction appears to be an important, yet insufficiently understood component of this network. Thyroid hormones play a crucial role in regulating metabolism, immune responses, and central nervous system function. Alterations in thyroid function, even within subclinical ranges, have been associated with mood disturbances and may share common inflammatory and metabolic pathways with depression. Furthermore, emerging data suggest that gut microbiota may influence thyroid hormone metabolism, including deiodinase activity, linking dysbiosis with thyroid axis dysregulation. Despite these insights, the integrated interactions between thyroid function, gut microbiota, metabolic syndrome, and inflammation in depression remain largely unexplored. This review explores current evidence to highlight gaps in existing research and synthesizes current knowledge, aiming to clarify mechanisms underlying immuno-metabolic depression. Understanding these relationships may provide a rationale for redefining depression as an immuno-metabolic disorder and support the development of more integrative therapeutic strategies targeting not only the brain, but also the gut-thyroid axis.
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Maternal sleep and psychological status in the postpartum period are associated with functional protein alterations in breast milk:a mother-infant cohort study.
BACKGROUND & AIMS: Postpartum sleep disorder and mental disorders are common unpleasant conditions faced by women after delivery, and they have many adverse effects on both mothers and infants. It is unclear whether breast milk composition is affected by maternal sleep, psychological state, diet and gut microbiome. This study aims to explore the effects of these key factors on the functional protein components of breast milk. METHODS: With a prospective design, this pilot study included a total of 41 postpartum women. Breast milk and maternal faecal samples collected at 42 days and 3 months postpartum were tested by liquid chromatography-mass spectrometry and 16S RNA sequencing, respectively. Sleep state, psychological state and dietary intake data were also collected from the mothers with validated questionnaires. RESULTS: In the early postpartum period, sleep disorders and depression were associated with a decrease in the functional proteins in breast milk. Disordered sleep was significantly negatively correlated with α-lactalbumin (cor = -0.578, p < 0.001), osteopontin (cor = -0.522, p < 0.01) and κ-casein (cor = -0.451, p < 0.01). Depression was negatively correlated with αs1-casein (cor = -0.422, p < 0.01), β-casein (cor = -0.317, p < 0.05) and casein (cor = -0.318, p < 0.05). In 3 months postpartum, most associations were disappeared. But a positive correlation was observed between β-casein (cor = 0.414, p < 0.01), casein (cor = 0.372, p < 0.05), total protein (cor = 0.376, p < 0.05) and depression, while a positive correlation was found between total protein (cor = 0.357, p < 0.05) and disordered sleep at 3 months postpartum. Faecal microbiome data illustrated that changes in the gut microbiome at early postpartum were associated with sleep disorders/depression, but not with the diet. Furthermore, functional pathway analysis revealed metabolic regulation in the amino acid synthesis and metabolic pathways associated with specific microbes was involved in the reduction of breast milk protein. CONCLUSION: Sleep disorders/depression could lead to significant changes in breast milk profiles at 42 days postpartum. Maternal gut microbiome might affect breast milk protein composition through regulating amino acid synthesis and metabolic pathways.
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Increased human intestinal barrier permeability plasma biomarkers zonulin and FABP2 correlated with plasma LPS and altered gut microbiome in anxiety or depression.
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Fecal microbiota in pediatric depression and its relation to bowel habits.
Although gut microbiota dysbiosis has been observed in the fecal samples of depressive adult patients, the detailed structure and composition of microbiota in pediatric depression remain unclear. To enhance our understanding of gut microbiota structure in depressive children, as well as the relationship between gut microbiota and bowel habits, we performed 16S rRNA sequencing to evaluate the gut microbial population in a cohort of 171 children (101 depressive patients and 70 controls) aged 12-18 years. Further analysis consisting of 30 drug-naive patients and 23 controls was performed to validate the results. Compared to controls, we found markedly decreased microbial richness and diversity, a distinct metagenomic composition with reduced short-chain fatty acid-producing bacteria (associated with healthy status), and overgrowth of bacteria such as Escherichia-Shigella and Flavonifractor in pediatric depression. Further analyses limited to drug-naive patients found similar results. Notably, we also observed that several taxa may be involved in the pathogenesis of disordered bowel habits in pediatric depression. Our findings suggest could inform future pediatric depression interventions specifically targeting the bacteria associated with bowel movements.
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Impact of Gut Microbiota on the Association between Diet and Depressive Symptoms in Breast Cancer.
Little is known about the relationship between diet and depression through the gut microbiota among breast cancer patients. This study aimed to examine the dietary intake differences between depressed breast cancer (DBC) and non-depressed breast cancer (NBC) patients, and whether the differences could lead to gut microbiota changes that affect depressive symptoms. Participants completed the Center for Epidemiological Studies-Depression Scale (CES-D) and 24 h dietary recall. Fecal samples of 18 DBC patients and 37 NBC patients were collected for next-generation sequencing. A total of 60 out of 205 breast cancer patients reported significant depressive symptoms suggested by a CES-D score ≥ 16, which might be related to lower intakes of energy, protein, dietary fiber, vitamin A, vitamin B2, niacin, calcium, phosphorus, potassium, iron, zinc, selenium, manganese and tryptophan, and a poor diet quality indicated by a lower total Chinese Healthy Eating Index (CHEI) score. Additionally, NBC patients demonstrated greater gut microbiota diversity and a healthier composition, in which the relative abundances of Proteobacteria and Escherichia-Shigella were both lower than in the DBC patients (p < 0.05). Alpha diversity was a significant mediator between diet quality and depression, while calcium, phosphorus and selenium significantly regulated depression independent of the gut microbiota. Breast cancer-related depressive symptoms might be associated with a poor diet quality via gut microbiota-dependent pathways and lower micronutrient intake via microbiota-independent pathways.
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Altered fecal microbiota composition in the Flinders sensitive line rat model of depression.
RATIONALE: The gut microbiota is increasingly recognized as a potential mediator of psychiatric diseases. Depressed patients have been shown to have a different microbiota composition compared with healthy controls, and several lines of research now aim to restore this dysbiosis. To develop novel treatments, preclinical models may provide novel mechanistic insights. OBJECTIVE AND METHODS: We characterized the gut microbiota of male adult Flinders sensitive line (FSL) rats, an animal model of depression, and their controls, Flinders resistant line (FRL) rats using 16S rRNA amplicon sequencing. Moreover, we performed fecal microbiota transplantation (using saline or pooled FRL/FSL feces) to study if the potential strain-specific differences could be transferred from one strain to the other, and if these differences were reflected in their depressive-like behavior in the forced swim test. RESULTS: FSL rats tended to have lower bacterial richness and altered relative abundances of several bacterial phyla, families, and species, including higher Proteobacteria and lower Elusimicrobia and Saccharibacteria. There was a clear separation between FRL and FSL rat strains, but no effect of treatment, i.e., the bacterial composition of FSL rats receiving FRL feces was still more similar to FSL and not FRL rats. Similarly, the transplantation did not reverse behavioral differences in the forced swim test, although FSL feces significantly increased immobility compared with saline. CONCLUSIONS: Our study showed that the gut microbiota composition of the depressive-like rats markedly differed from their controls, which may be of value for future microbiota-targeted work in this and similar animal models.