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The Role of Microbiome in Insomnia, Circadian Disturbance and Depression.
Good sleep and mood are important for health and for keeping active. Numerous studies have suggested that the incidence of insomnia and depressive disorder are linked to biological rhythms, immune function, and nutrient metabolism, but the exact mechanism is not yet clear. There is considerable evidence showing that the gut microbiome not only affects the digestive, metabolic, and immune functions of the host but also regulates host sleep and mental states through the microbiome-gut-brain axis. Preliminary evidence indicates that microorganisms and circadian genes can interact with each other. The characteristics of the gastrointestinal microbiome and metabolism are related to the host's sleep and circadian rhythm. Moreover, emotion and physiological stress can also affect the composition of the gut microorganisms. The gut microbiome and inflammation may be linked to sleep loss, circadian misalignment, affective disorders, and metabolic disease. In this review article, we discuss various functions of the gut microbiome and how its activities interact with the circadian rhythms and emotions of the host. Exploring the effects of the gut microbiome on insomnia and depression will help further our understanding of the pathogenesis of mental disorders. It is therefore important to regulate and maintain a normal gastrointestinal micro-ecological environment in patients when treating mental disorders.
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Time-restricted feeding causes irreversible metabolic disorders and gut microbiota shift in pediatric mice.
BACKGROUND: Time-restricted feeding regimen (TRF), that is, no food consumption for 14-16 h during the light phase per day, attenuates the fattening traits and metabolic disorders in adults. This study aims to further investigate whether TRF would be protective against similar nutritional challenges in juvenile mice. METHODS: Mice in the experimental group were treated with TRF during the first 4 weeks (considered to be the childhood phase of mice) before switching to ad libitum (AD) feeding pattern as adults; the control group with all subjects sticks to AD mode. Body weight was monitored, and serum biochemistry, sexual maturity, immune function, and gut microbiota were assessed at a certain timing. RESULTS: Mice treated with TRF during the childhood period (from weaning age) but went through AD feeding pattern as adults demonstrated the tendency of higher body weight, higher levels of serum glucose, shrunken Langerhans islets, fatty liver disease, thickening of aortic walls, delayed sexual development, increased proportion of T regulatory cells, and unhealthy gut microbiota. CONCLUSION: Childhood TRF causes pleiotropic adverse effects, including severe irreversible metabolic disorders, depressed immune function, and retarded puberty. Microbiota set the stage for TRF to employ downstream reactions on the above changes.
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Probiotics therapy show significant improvement in obesity and neurobehavioral disorders symptoms.
Obesity is a complex metabolic disease, with cognitive impairment being an essential complication. Gut microbiota differs markedly between individuals with and without obesity. The microbial-gut-brain axis is an important pathway through which metabolic factors, such as obesity, affect the brain. Probiotics have been shown to alleviate symptoms associated with obesity and neurobehavioral disorders. In this review, we evaluated previously published studies on the effectiveness of probiotic interventions in reducing cognitive impairment, depression, and anxiety associated with obesity or a high-fat diet. Most of the probiotics studied have beneficial health effects on obesity-induced cognitive impairment and anxiety. They positively affect immune regulation, the hypothalamic-pituitary-adrenal axis, hippocampal function, intestinal mucosa protection, and glucolipid metabolism regulation. Probiotics can influence changes in the composition of the gut microbiota and the ratio between various flora. However, probiotics should be used with caution, particularly in healthy individuals. Future research should further explore the mechanisms underlying the gut-brain axis, obesity, and cognitive function while overcoming the significant variation in study design and high risk of bias in the current evidence.
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Gut Microbiota and Bipolar Disorder: An Overview on a Novel Biomarker for Diagnosis and Treatment.
The gut microbiota is the set of microorganisms that colonize the gastrointestinal tract of living creatures, establishing a bidirectional symbiotic relationship that is essential for maintaining homeostasis, for their growth and digestive processes. Growing evidence supports its involvement in the intercommunication system between the gut and the brain, so that it is called the gut-brain-microbiota axis. It is involved in the regulation of the functions of the Central Nervous System (CNS), behavior, mood and anxiety and, therefore, its implication in the pathogenesis of neuropsychiatric disorders. In this paper, we focused on the possible correlations between the gut microbiota and Bipolar Disorder (BD), in order to determine its role in the pathogenesis and in the clinical management of BD. Current literature supports a possible relationship between the compositional alterations of the intestinal microbiota and BD. Moreover, due to its impact on psychopharmacological treatment absorption, by acting on the composition of the microbiota beneficial effects can be obtained on BD symptoms. Finally, we discussed the potential of correcting gut microbiota alteration as a novel augmentation strategy in BD. Future studies are necessary to better clarify the relevance of gut microbiota alterations as state and disease biomarkers of BD.
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Stress-induced despair behavior develops independently of the Ahr-RORγt axis in CD4 + cells.
Current treatments for major depressive disorder are limited to neuropharmacological approaches and are ineffective for large numbers of patients. Recently, alternative means have been explored to understand the etiology of depression. Specifically, changes in the microbiome and immune system have been observed in both clinical settings and in mouse models. As such, microbial supplements and probiotics have become a target for potential therapeutics. A current hypothesis for the mechanism of action of these supplements is via the aryl hydrocarbon receptor's (Ahr) modulation of the T helper 17 cell (Th17) and T regulatory cell axis. As inflammatory RORγt + CD4 + Th17 T cells and their primary cytokine IL-17 have been implicated in the development of stress-induced depression, the connection between stress, the Ahr, Th17s and depression remains critical to understanding mood disorders. Here, we utilize genetic knockouts to examine the role of the microbial sensor Ahr in the development of stressinduced despair behavior. We observe an Ahr-independent increase in gut-associated Th17s in stressed mice, indicating that the Ahr is not responsible for this communication. Further, we utilized a CD4-specific RAR Related Orphan Receptor C (Rorc) knockout line to disrupt the production of Th17s. Mice lacking Rorc-produced IL-17 did not show any differences in behavior before or after stress when compared to controls. Finally, we utilize an unsupervised machine learning system to examine minute differences in behavior that could not be observed by traditional behavioral assays. Our data demonstrate that neither CD4 specific Ahr nor Rorc are necessary for the development of stress-induced anxiety- or depressive-like behaviors. These data suggest that research approaches should focus on other sources or sites of IL-17 production in stress-induced depression.
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Yak milk ameliorates chronic alcohol-induced brain injury in mice by modulating the gut microbiota and suppressing the TLR4/NF-κB pathway.
This study investigated the protective effects of yak milk (YM) on chronic alcohol-related brain injury (ARBI) in mice. The findings revealed that YM intake significantly alleviated alcohol-induced anxiety-like behaviors, and offered protection against ARBI by decreasing oxidative stress and suppressing the inflammatory response in the brain tissues. Notably, the effects were more pronounced in the high-dose yak milk (HY) group compared to the low-dose yak milk (LY) and high-dose regular cow's milk (HM) groups. Additionally, YM was found to influence the gut microbiota in mice, particularly in relation to microorganisms associated with neuroinflammation and depressive behaviors, such as Parabacteroides and Alistipes. Metabolite analysis revealed that the levels of linoleic acid, N-arachidonoyl dopamine, norlobaridone, epothilone A, xanthotoxol, and indoprofen were significantly elevated in the HY group. Furthermore, KEGG analysis suggested that YM intervention primarily affected the pathways of ABC transporters, cysteine and methionine metabolism. Subsequently, western blot analysis confirmed that this intervention inhibited TLR4 and NF-κB p65 protein levels, leading to a reduction in inflammatory expression. Therefore, we propose that YM provides protection against ARBI and anxiety-like behaviors in mice by modulating oxidative stress, influencing the expression of inflammatory mediators associated with the TLR4/NF-κB pathway, and regulating the gut microbiota and metabolic processes through the "gut-brain" axis.
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Gut dysbiosis mediates neurotoxic effects of environmentally relevant tylosin exposure in adult zebrafish.
Tylosin, a widely used veterinary macrolide antibiotic, raises environmental concerns due to its persistence and potential health risks. However, the neurotoxic effects of chronic low-dose tylosin exposure remain unclear. This study assessed the neurotoxicity of chronic exposure to environmentally relevant tylosin concentrations (5000 ng/L) in adult zebrafish. Behavioral tests indicated anxiety- and depression-like behaviors, including reduced exploration and increased freezing. Histopathology revealed neuronal degeneration, evidenced by decreased Nissl staining in key brain areas. Transcriptomic analysis identified significant changes in genes related to neuroinflammation, synaptic dysfunction, immune response, and steroid metabolism. Multi-omics approaches further showed substantial alterations in gut microbiota composition and metabolic profiles, particularly involving tryptophan metabolism and steroid hormone synthesis. These gut changes correlated with impaired intestinal barrier function, including fewer goblet cells and reduced tight junction and mucin-2 protein expression. Fecal microbiota transplantation confirmed the role of altered gut microbiota in inducing anxiety- and depression-like behaviors, highlighting microbiota-gut-brain axis involvement. Molecular docking identified microbial metabolites (MG 20:4, 2E-dodecenedioic acid, Ononin) interacting with critical neurodevelopmental and stress-response proteins (LRAT, BHLHE40, HSPA5), potentially linking microbiota shifts to brain dysfunction. Our results demonstrate that chronic environmental tylosin exposure induces neurotoxicity through gut dysbiosis and compromised intestinal barriers, disrupting essential neuroactive pathways. These findings emphasize the importance of considering microbiota-gut-brain axis disruption in environmental antibiotic risk assessments.
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Microbiota and parasite relationship.
The diversity of microbiota is different in each person. Many health problems such as autoimmune diseases, diabetes, cardiovascular diseases, and depression can be caused by microbiota imbalance. Since the parasite needs a host to survive, it interacts closely with the microbiota elements. Blastocystis acts on the inflammatory state of the intestine and may cause various gastrointestinal symptoms, on the contrary, it is more important for gut health because it causes bacterial diversity and richness. Blastocystis is associated with changes in gut microbiota composition, the ultimate indicator of which is the Firmicutes/Bacteroidetes ratio. The Bifidobacterium genus was significantly reduced in IBS patients and Blastocystis, and there is a significant decrease in Faecalibacterium prausnitzii, which has anti-inflammatory properties in Blastocystis infection without IBS. Lactobacillus species reduce the presence of Giardia, and the produced bacteriocins prevent parasite adhesion. The presence of helminths has been strongly associated with the transition from Bacteroidetes to Firmicutes and Clostridia. Contrary to Ascaris, alpha diversity in the intestinal microbiota decreases in chronic Trichuris muris infection, and growth and nutrient metabolism efficiency can be suppressed. Helminth infections indirectly affect mood and behavior in children through their effects on microbiota change. The main and focus of this review is to address the relationship of parasites with microbiota elements and to review the data about what changes they cause. Microbiota studies have gained importance recently and it is thought that it will contribute to the treatment of many diseases as well as in the fight against parasitic diseases in the future.
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Intricate mechanism of anxiety disorder, recognizing the potential role of gut microbiota and therapeutic interventions.
Anxiety is a widespread psychological disorder affecting both humans and animals. It is a typical stress reaction; however, its longer persistence can cause severe health disorders affecting the day-to-day life activities of individuals. An intriguing facet of the anxiety-related disorder can be addressed better by investigating the role of neurotransmitters in regulating emotions, provoking anxiety, analyzing the cross-talks between neurotransmitters, and, most importantly, identifying the biomarkers of the anxiety. Recent years have witnessed the potential role of the gut microbiota in human health and disorders, including anxiety. Animal models are commonly used to study anxiety disorder as they offer a simpler and more controlled environment than humans. Ultimately, developing new strategies for diagnosing and treating anxiety is of paramount interest to medical scientists. Altogether, this review article shall highlight the intricate mechanisms of anxiety while emphasizing the emerging role of gut microbiota in regulating metabolic pathways through various interaction networks in the host. In addition, the review will foster information about the therapeutic interventions of the anxiety and related disorder.
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Tryptophan Metabolism Disorder-Triggered Diseases, Mechanisms, and Therapeutic Strategies: A Scientometric Review.
BACKGROUND: Tryptophan is widely present in foods such as peanuts, milk, and bananas, playing a crucial role in maintaining metabolic homeostasis in health and disease. Tryptophan metabolism is involved in the development and progression of immune, nervous, and digestive system diseases. Although some excellent reviews on tryptophan metabolism exist, there has been no systematic scientometric study as of yet. METHODS: This review provides and summarizes research hotspots and potential future directions by analyzing annual publications, topics, keywords, and highly cited papers sourced from Web of Science spanning 1964 to 2022. RESULTS: This review provides a scientometric overview of tryptophan metabolism disorder-triggered diseases, mechanisms, and therapeutic strategies. CONCLUSIONS: The gut microbiota regulates gut permeability, inflammation, and host immunity by directly converting tryptophan to indole and its derivatives. Gut microbial metabolites regulate tryptophan metabolism by activating specific receptors or enzymes. Additionally, the kynurenine (KYN) pathway, activated by indoleamine-2, 3-dioxygenase (IDO) and tryptophan 2, 3-dioxygenase, affects the migration and invasion of glioma cells and the development of COVID-19 and depression. The research and development of IDO inhibitors help to improve the effectiveness of immunotherapy. Tryptophan metabolites as potential markers are used for disease therapy, guiding clinical decision-making. Tryptophan metabolites serve as targets to provide a new promising strategy for neuroprotective/neurotoxic imbalance affecting brain structure and function. In summary, this review provides valuable guidance for the basic research and clinical application of tryptophan metabolism.