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Revisit gut microbiota and its impact on human health and disease.
Trillions of microbes have evolved with and continue to live on human beings. With the rapid advances in tools and technology in recent years, new knowledge and insight in cross-talk between the microbes and their hosts have gained. It is the aim of this work to critically review and summarize recent literature reports on the role of microbiota and mechanisms involved in the progress and development of major human diseases, which include obesity, hypertension, cardiovascular disease, diabetes, cancer, Inflammatory Bowel Disease (IBD), gout, depression and arthritis, as well as infant health and longevity.
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Roudoukou-Suanzaoren Ameliorates Chronic Restraint-Induced Anxiety- and Depression-Like Behaviors in Mice via the Gut-Brain Axis.
Anxiety and depression are growing global burdens with limited drug options. Traditional Chinese medicine (TCM) offers unique advantages, including Roudoukou-Suanzaoren (RS), an ancient TCM-derived beverage with the potential for treating these conditions. This study aims to explore whether this combination improves the outcomes. The results show that the main constituents of RS include flavonoids, terpenoids, alkaloids, and phenylpropanoids. Behavioral and histopathological analyses demonstrate that RS alleviates chronic restraint stress (CRS)-induced anxiety- and depression-like behaviors and attenuates neuropathological damage in relevant brain regions; the underlying mechanism is likely mediated by the CREB/BDNF/TrkB signaling pathway. Meanwhile, RS reduces proinflammatory cytokines in tissues, decreases hippocampal microglial numbers, and increases astrocytes. Additionally, RS attenuates colonic injury, restores intestinal permeability, upregulates tight-junction proteins, and improves gut microbiota dysbiosis. This study highlights that RS exerts antianxiety and antidepression effects by modulating the gut microbiota, controlling inflammatory responses, and increasing BDNF levels through the "gut-brain axis" pathway.
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Agmatine modulation of gut-brain axis alleviates dysbiosis-induced depression-like behavior in rats.
Depression is a global health concern affecting nearly 280 million individuals. It not only imposes a significant burden on economies and healthcare systems but also manifests complex physiological connections and consequences. Agmatine, a putative neuromodulator derived primarily from beneficial gut microbes specially Lactobacillus, has emerged as a potential therapeutic agent for mental health. 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 agmatine. Therefore, this study aimed to investigate the potential mechanism of agmatine in antibiotic-induced dysbiosis and depression-like behavior in rats, focusing on its modulation of the gut-brain axis. Depression-like behavior associated with dysbiosis was induced through a seven-day regimen of the broad-spectrum antibiotic, comprising ampicillin and metronidazole and validated through microbial, biochemical, and behavioral alterations. On day 8, antibiotic-treated rats exhibited loose fecal consistency, altered fecal microbiota, and depression-like behavior in forced swim test. Pro-inflammatory cytokines were elevated, while agmatine and monoamine levels decreased in the hippocampus and prefrontal cortex. Antibiotic administration disrupted tight junction proteins in the ileum, affecting gut architecture. Oral administration of agmatine alone or combined with probiotics significantly reversed antibiotic-induced dysbiosis, restoring gut microbiota and mitigating depression-like behaviors. This intervention also restored neuro-inflammatory markers, increased agmatine and monoamine levels, and preserved gut integrity. The study highlights the regulatory role of endogenous agmatine in the gut-brain axis in broad-spectrum antibiotic induced dysbiosis and associated depression-like behavior.
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Plant Hormones: Key Players in Gut Microbiota and Human Diseases?
It is well established that plant hormones such as auxins, cytokinins (CKs), and abscisic acid (ABA) not only govern important plant physiological traits but are key players in plant-microbe interactions. A poorly appreciated fact, however, is that both microbes and animals produce and perceive plant hormones and their mimics. Moreover, dietary plant hormones impact on human physiological process such as glucose assimilation, inflammation, and cell division. This leads us to wonder whether plant hormones could ensure functions in microbes per se as well as in animal-microbe interactions. We propose here and explore the hypothesis that plant hormones play roles in animal-microbiota relationships, with consequences for human health.
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Insights into a possible role of glucagon-like peptide-1 receptor agonists in the treatment of depression.
Depression is a highly prevalent mood disorder and one of the major health concerns in modern society. Moreover, it is characterized by a high prevalence of coexistence with many other diseases including metabolic disorders such as type 2 diabetes mellitus (T2DM) and obesity. Currently used antidepressant drugs, which mostly target brain monoaminergic neurotransmission, have limited clinical efficacy. Although the etiology of depression has not been fully elucidated, current scientific data emphasize the role of neurotrophic factors deficiencies, disturbed homeostasis between the nervous system and the immune and endocrine systems, as well as disturbances in brain energy metabolism and dysfunctions in the gut-brain axis as important factors in the pathogenesis of this neuropsychiatric disorder. Therefore, therapeutic options that could work in a way other than classic antidepressants are being sought to increase the effectiveness of the treatment. Interestingly, glucagon-like peptide-1 receptor agonists (GLP-1RAs), used in the treatment of T2DM and obesity, are known to show pro-cognitive and neuroprotective properties, and exert modulatory effects on immune, endocrine and metabolic processes in the central nervous system. This review article discusses the potential antidepressant effects of GLP-1RAs, especially in the context of their action on the processes related to neuroprotection, inflammation, stress response, energy metabolism, gut-brain crosstalk and the stability of the gut microbiota.
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Chronic exposure to metam sodium-based pesticide in mice during adulthood elevated anxiety and depression-like behaviors: Involvement of serotoninergic depletion and gut microbiota dysbiosis.
Metam sodium-based pesticide (MS-BP) is widely used in agriculture and public health. We have previously demonstrated that maternal exposure to MS-BP resulted in sensorimotor alterations in mice offspring with long-lasting deficits including anxiety- and depression-like behaviors. Here, we project to verify whether these two neurobehavioral effects occur during adulthood following direct exposure to MS-BP and whether it results in changes in the serotoninergic system and gut microbiota. Our findings showed that chronic exposure to MS-BP increased anxiety- and depression-like behaviors, accompanied by a depletion of serotonin-like neurons within the dorsal raphe nucleus and a reduction in serotoninergic terminals in the infralimbic cortex and the basolateral amygdala. In addition, all MS-BP-exposed animals exhibited a reduced total bacterial number and diversity of gut microbiota. Taken together, our data demonstrated that MS-BP-induced behavioral changes could be related to the impairment of the serotoninergic system and gut microbiota dysbiosis.
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Buspirone alleviates anxiety, depression, and colitis; and modulates gut microbiota in mice.
Gut microbiota regulate the neurodevelopmental processes and brain functions through the regulation of the microbiota-gut interaction and gut-brain communication. Buspirone, an agonist for serotonin 5-HT1A receptors, is used for the treatment of anxiety/depression. Therefore, to understand the gut microbiota-mediated mechanism of buspirone on anxiety/depression, we examined its effect on the immobilization stress (IS) or Escherichia coli K1 (EC)-induced anxiety/depression in mice. Oral or intraperitoneal administration of buspirone significantly suppressed stressor-induced anxiety/depression-like behaviors in the elevated plus maze, light/dark transition, tail suspension, and forced swimming tasks. Their treatments also reduced TNF-α expression and NF-κB+/Iba1+ cell population in the hippocampus and myeloperoxidase activity and NF-κB+/CD11c+ cell population in the colon. Buspirone treatments partially restored IS- or EC-induced gut microbiota perturbation such as β-diversity to those of normal control mice: they reduced the IS- or EC-induced gut Proteobacteria population. In particular, the anxiolytic activity of buspirone was positively correlated with the populations of Bacteroides and PAC001066_g in EC- or IS-exposed mice, while the populations of Lachnospiraceae, KE159660_g, LLKB_g, Helicobacter, and PAC001228_g were negatively correlated. The anti-depressant effect of buspirone was positively correlated with the Roseburia population. The fecal microbiota transplantations from buspirone-treated mice with IS-induced anxiety/depression or normal control mice suppressed IS-induced anxiety/depression-like behaviors and reduced hippocampal NF-κB+/Iba1+ and colonic NF-κB+/CD11c+ cell populations in the transplanted mice. Furthermore, they modified IS-induced perturbation of gut microbiota composition, particularly Proteobacteria, in the transplanted mice. In conclusion, buspirone alleviates IS as well as EC-induced anxiety/depression and colitis. It also suppresses associated neuroinflammation and modulates gut microbiota. Future studies can help to explain the relationship, if any, in the central and peripheral effects of buspirone.
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[Advances in the application of fecal microbiota transplantation for the treatment of nervous system diseases].
The intestinal microbiota exhibits a strong correlation with the function of the central nervous system, exerting influence on the host brain through neural pathways, immune pathways, and microbial metabolites along the gut-brain axis. Disorders in the composition of the intestinal microbial are closely associated with the onset and progression of neurological disorders, such as depression, Alzheimer's disease, and Parkinson's disease. It has been proven that fecal microbiota transplantation can improve symptoms in animal models of neurological diseases and clinical patients. This paper provides a comprehensive review of the composition and function of the human intestinal microbiota, as well as the intricate the relationship between the human intestinal microbiota and nervous system diseases through the gut-brain axis. Additionally, it delves into the research advancements and underlying mechanism of fecal microbiota transplantation in the treatment of nervous system diseases. These findings offer novel insights and potential avenues for clinical interventions targeting nervous system diseases.
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[The regulatory role of gut microbiota in inflammation in depression and anxiety].
Numerous studies have identified the important role of the gut microbiota in maintaining of the CNS normal functioning and in the pathogenesis of mental disorders as one of the systems regulating the bidirectional communication between the gut and the brain. The microbiota has been found to be involved in the modulation of inflammation as well as in the development and function of the immune and nervous systems. It is assumed that in multicellular organisms, the nervous and immune systems have evolved together with the microbiota, being in interaction with it, in order to optimize the body's ability to adapt to a wide range of environmental stresses in order to maintain the constancy of its homeostasis. Normally, microbes live in stable communities, while under conditions of even mild or chronic social stress, significant shifts in the composition of the microbiota occur, which lead to the development of dysbiosis associated with changes in microbiota metabolites, which can lead to the formation of physiology and behavior characteristic of stress and depression. Microbes influence the activation of peripheral immune cells that regulate the response to neuroinflammation, brain damage, autoimmune responses, and neurogenesis. The review provides a brief overview of the normal gut microbiota, describes the factors influencing the state of the microbiota, and also discusses recent discoveries concerning the regulatory effect of the gut microbiota on CNS functions, the immune system, and inflammation in the pathogenesis of depression and anxiety.
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The microbiota-gut-brain axis and its modulation in the therapy of depression: Comparison of efficacy of conventional drugs and traditional Chinese medicine approaches.
Depression is a common and severe mental disease that places a heavy burden on human society, which can lead to decreased cognitive function, energy loss, insomnia, and even suicide. Although medication plays an important role in improving the symptoms of depression, approximately one third of people with depression do not significantly benefit from medication and experience various adverse reactions. Recently, increasing evidence has shown that gut microbes play an important role in the occurrence and development of depression. There have been illuminating studies previously conducted on the relationship between antidepressant chemicals, traditional Chinese medicine, and the microbiota-gut-brain axis (MGBA). Therefore, in this review, we summarize the role of the MGBA in the occurrence and development of depression, especially the important role of the MGBA in the mechanism of action of antidepressants. Modulation of the MGBA is proposed to enhance the efficacy of antidepressant drugs and reduce their side effects and disease recurrence, so as to provide a new method for the treatment of depression.