Your browser does not allow saving data (e.g. private mode): bookmarks will be lost when the tab closes.
Search PubMed
Keywords, author, journal, years — results from PubMed, abstracts with Russian translation, bookmarks in your browser.
Found: 3 214
Page 285 of 322-
Paraburkholderia sabiae administration alters zebrafish anxiety-like behavior via gut microbial taurine metabolism.
Interventions to the gut microbiome manipulate the gut-brain axis and could be useful in the treatment of anxiety and depression. In this study, we demonstrated that administration of the bacterium Paraburkholderia sabiae reduces anxiety-like behavior in adult zebrafish. P. sabiae administration increased the diversity of the zebrafish gut microbiome. Linear discriminant analysis Effect Size (LEfSe) analysis revealed that the populations of Actinomycetales including Nocardiaceae, Nocardia, Gordoniaceae, Gordonia, Nakamurellaceae, and Aeromonadaceae were reduced, whereas those of Rhizobiales including Xanthobacteraceae, Bradyrhizobiaceae, Rhodospirillaceae, and Pirellulaceae were increased in the gut microbiome. Functional analysis using Phylogenetic Investigation of Communities by Reconstruction of Unobserved States (PICRUSt2) predicted that P. sabiae administration altered taurine metabolism in the zebrafish gut, and we demonstrated that P. sabiae administration increased the taurine concentration in the brain. Since taurine functions as an antidepressant neurotransmitter in vertebrates, our results suggest that P. sabiae could improve anxiety-like behavior in zebrafish via the gut-brain axis.
-
Gut Feelings: How Microbes, Diet, and Host Immunity Shape Disease.
The human gut microbiome is intricately linked to systemic and organ-specific immune responses and is highly responsive to dietary modulation. As metagenomic techniques enable in-depth study of an ever-growing number of gut microbial species, it has become increasingly feasible to decipher the specific functions of the gut microbiome and how they may be modulated by diet. Diet exerts both supportive and selective pressures on the gut microbiome by regulating a multitude of factors, including energy density, macronutrient and micronutrient content, and circadian rhythm. The microbiome, in turn, contributes to local and systemic immune responses by providing colonization resistance against pathogens, shaping immune cell activity and differentiation, and facilitating the production of bioactive metabolites. Emerging research has strengthened the connections between the gut microbiome and cardiometabolic disorders (e.g., cardiovascular disease, obesity, type-2 diabetes), autoimmune conditions (e.g., type-1 diabetes, rheumatoid arthritis, celiac disease), respiratory disease, chronic kidney and liver disease, inflammatory bowel disease, and neurological disorders (e.g., Alzheimer's, Parkinson's disease, depressive disorders). Here, we outline ways in which dietary factors impact host response in diseases through alterations of gut microbiome functionality and composition. Consideration of diet-mediated microbial effects within the context of the diseases discussed highlights the potential of microbiome-targeted treatment strategies as alternative or adjunct therapies to improve patient outcomes.
-
Mental health and gut-brain crosstalk: implications for depression and Alzheimer's disease.
Brain health and mental health disorders are increasingly becoming an essential priority for modern societies as they affect different parameters of life, such as brain health, quality of life, and productivity with a heavy societal and economic burden. Among mental health disorders, depression and Alzheimer disease (AD) have the higher impact on mental health globally as they are highly prevalent, cause long-term cognitive and mood deficits while they are deeply interconnected, with chronic stress raising as a risk factor and potential link between both disorders. This review focuses on the gut-brain axis, a bidirectional communication network that links the gut microbiome with the central nervous system, and its role in brain malfunction and pathology related to stress, depression and AD. This intricate gut-brain crosstalk is orchestrated through top-down and bottom-up mechanisms implicating the HPA axis, the enteric nervous system as well as gut microbiota-derived metabolites, neurotransmitters, epigenetic processes and extracellular vesicles/exosomes that can contribute to depression and AD. The current work provides a comprehensive summary of evidence linking gut microbial alterations to these brain pathologies, with particular focus on lifestyle and nutrition (e.g. food, water) as critical regulators. Lastly, we explore the therapeutic potential of microbiome-targeted interventions including pro/pre/post-biotics, and trace elements (e.g. lithium and silicon). Overall, this review highlights the potential of microbiome-centered strategies as novel interventions to support mental health and wellbeing.
-
Fibre-rich diet attenuates chemotherapy-related neuroinflammation in mice.
The gastrointestinal microbiota has received increasing recognition as a key mediator of neurological conditions with neuroinflammatory features, through its production of the bioactive metabolites, short-chain fatty acids (SCFAs). Although neuroinflammation is a hallmark shared by the neuropsychological complications of chemotherapy (including cognitive impairment, fatigue and depression), the use of microbial-based therapeutics has not previously been studied in this setting. Therefore, we aimed to investigate the effect of a high fibre diet known to modulate the microbiota, and its associated metabolome, on neuroinflammation caused by the common chemotherapeutic agent 5-fluorouracil (5-FU). Twenty-four female C57Bl/6 mice were treated with 5-FU (400 mg/kg, intraperitoneal, i.p.) or vehicle control, with or without a high fibre diet (constituting amylose starch; 4.7 % crude fibre content), given one week prior to 5-FU and until study completion (16 days after 5-FU). Faecal pellets were collected longitudinally for 16S rRNA gene sequencing and terminal SCFA concentrations of the caecal contents were quantified using gas chromatography-mass spectrometry (GC-MS). Neuroinflammation was determined by immunofluorescent analysis of astrocyte density (GFAP). The high fibre diet significantly altered gut microbiota composition, increasing the abundance of Bacteroidaceae and Akkermansiaceae (p < 0.0001 and p = 0.0179) whilst increasing the production of propionate (p = 0.0097). In the context of 5-FU, the diet reduced GFAP expression in the CA1 region of the hippocampus (p < 0.0001) as well as the midbrain (p = 0.0216). Astrocyte density negatively correlated with propionate concentrations and the abundance of Bacteroidaceae and Akkermansiaceae, suggesting a relationship between neuroinflammatory and gastrointestinal markers in this model. This study provides the first evidence of the neuroprotective effects of fibre via dietary intake in alleviating the neuroimmune changes seen in response to systemically administered 5-FU, indicating that the microbiota-gut-brain axis is a targetable mediator to reduce the neurotoxic effects of chemotherapy treatment.
-
Effects of chronic allergic lung inflammation on gut microbiota and depression-like behavior in mice.
AIM: Emerging epidemiological studies have reported a link between allergic diseases, including asthma, and depression. Evidently, the gut microbiota is involved in the pathogenesis of asthma and depression. Therefore, we investigated whether allergic lung inflammation in mice causes gut microbial dysbiosis, via the gut-brain axis, which is potentially associated with depression. METHODS: Wild-type C57BL/6J female mice were sensitized with intranasal house dust mite (HDM) antigen or phosphate-buffered saline (PBS) for 6 weeks to induce chronic allergic lung inflammation. Sucrose preference tests were performed for assessing depression. Fecal samples were collected, and 16S ribosomal RNA gene sequencing was performed to detect differences in gut microbiota composition between the HDM and PBS groups. The distance calculation, clustering of operational taxonomic units, rarefaction analysis, and estimator calculation (α- and β-diversity) were performed. RESULTS: There was a significant difference in β-diversity (Bray-Curtis dissimilarity, F-statistics = 6.16, p = 0.001) of the gut microbiota between HDM and PBS groups. However, there was no difference in the α-diversity. We observed multiple differentially abundant bacteria in the HDM and PBS groups. The order class Clostridia (p = 0.0036) and genus Faecalibaculum (p = 0.028) were more abundant in the HDM group, whereas the phylum Firmicutes (p = 0.037) and genera Dubosiella (p = 0.00024) and Turicibacter (p = 0.037) were more abundant in the PBS group. Notably, the relative abundance of some bacteria was correlated with the sucrose preference test results. CONCLUSIONS: Six weeks of intranasal HDM administration to mimic the chronic status of lung inflammation in asthma changed the gut microbiome in mice and was associated with depression-like behavioral changes.
-
The microbiota-gut-brain-epigenome axis as a novel therapeutic target for decoding postpartum depression.
BACKGROUND: Postpartum depression (PPD) is a psychological disorder affecting approximately 10-15% of women following childbirth, with significant implications for maternal and infant well-being. While hormonal fluctuations and psychosocial factors have long been considered primary contributors, recent reports demonstrated that gut microbiome is implicated in modulating maternal mood and behavior. The bidirectional communication between the gut and brain, mediated by microbiota-gut-brain axis, along with genetic and epigenetic modifications, has gained increasing attention as a potential mechanistic pathway in PPD. However, the precise genetic and epigenetic underpinnings of this interaction remain to be elucidated. OBJECTIVE: This review aims to explore the genetic and epigenetic landscape of postpartum depression, with a significant focus pertinent to gut microbiota role in shaping neurobiological outcomes. By integrating recent findings from genomic, epigenomic, and microbiome research, we seek to elucidate novel mechanistic insights and potential therapeutic avenues. METHODS: A comprehensive literature search was conducted using public databases, including PubMed, Google Scholar, and NCBI, to identify relevant studies on PPD, gut microbiota, genetics, and epigenetics. RESULTS: Gut microbiota and neuroimmune modulation: peripartum changes in gut microbiota composition have been linked to immune dysregulation, inflammation, and neurotransmitter imbalances, all of which are implicated in PPD pathophysiology. Genetics and epigenetics of PPD: Genome-wide association studies (GWAS) revealed a profound genetic risk loci associated with PPD. Additionally, DNA methylation, histone modifications, and non-coding RNAs have profound functional implications in gene expression regulation, influencing PPD susceptibility. Epigenetic influence of the gut microbiome: The gut microbiome affects epigenetic modifications, such as DNA methylation and histone acetylation, which may lead to fetal programming and maternal mental health disorders. Choline metabolism and maternal mental health: Choline, an essential nutrient involved in epigenetic regulation, influences gut microbiota composition and brain function. Dysregulation in choline metabolism is associated with higher risk of PPD. Clinical and therapeutic implications: Understanding the genetic and epigenetic mechanisms underlying PPD offers new avenues for personalized therapeutic interventions, including probiotic and prebiotic strategies, microbiome-based treatments, and targeted epigenetic therapies. CONCLUSION: The interplay between genetics, epigenetics, and gut microbiota represents a novel and promising area of research in understanding postpartum depression. The microbiota-gut-brain axis serves as a crucial mediator in this relationship, influencing neuroimmune regulation, neurotransmitter synthesis, and epigenetic modifications. Future studies should focus on integrating multi-omics approaches to unravel the molecular complexity of PPD and develop targeted interventions aimed at restoring microbiome and epigenetic homeostasis.
-
Magnesium Orotate and the Microbiome-Gut-Brain Axis Modulation: New Approaches in Psychological Comorbidities of Gastrointestinal Functional Disorders.
Magnesium orotate has been cited in the medical literature for the past three years as a possible adjuvant in some pediatric and adult gastroenterological disorders associated with dysbiosis. Studies also focus on the possibility of adding magnesium orotate in psychiatric disorders' treatment, such as major depression and anxiety. The most relevant element in these studies is the efficiency of magnesium orotate therapy in cases with both gastroenterological and psychiatric symptoms. This article proposes a literature review, focused on the studies published in the last three years, targeting magnesium orotate treatment and probiotic supplementation in patients with both digestive and psychiatric symptoms. Moreover, this review will compare the efficiency of magnesium orotate and probiotics within both the pediatric and adult communities, focusing on the possibility of gut-brain axis modulation and its involvement in the clinical evolution of these patients.
-
Identifying and ranking causal association between gut microbiota and neuroticism.
BACKGROUND: Recent studies had explored that gut microbiota was associated with personality traits through the gut-brain axis. Nevertheless, the fundamental causality remained obscure. METHODS: Mendelian randomization (MR) was used to investigate the causal relationship between gut microbiota, metabolites and neuroticism-related traits. Summary data-based Mendelian randomization (SMR) was utilized to identify genes associated pleiotropically with microbial taxa. RESULTS: MR analyses identified reliable causal evidence of 20 bacterial taxa related to neuroticism and its worry or depressed affect sub-cluster. A higher relative abundance of the Ruminococcus gauvreauii genus was associated with a higher risk of neuroticism [odds ratio (OR) = 1.04, 95% CI: 1.02-1.06, P = 2.85 × 10-3], depressed affect [OR = 1.04, 95% CI: 1.02-1.06, P = 5.50 × 10-3] and worry (OR = 1.04, 95% CI: 1.02-1.06, P = 7.81 × 10-4), respectively. We identified the probes tagging CPSF1, that showed pleiotropic association with Ruminococcus gauvreauii in brain or colon tissues. Finally, we provided evidence that Ruminococcus gauvreauii present causal association with the neurotransmitter such as glutamine and glutamate. CONCLUSIONS: This study implied a causal relationship between the gut microbiome composition, metabolites and neuroticism, thus providing novel insights into the gut microbiota-mediated development mechanism of neuroticism.
-
Four Decades of Stress, Depression, and Close Relationships: Lessons from Psychoneuroimmunology.
Human psychoneuroimmunology research has demonstrated that stress, depression, and close relationships reliably shape immune and endocrine function in ways that matter for health. Across studies of examination stress, laboratory stressors, marital discord, cancer survivorship, and dementia caregiving, psychosocial adversity predicts more infections, weaker vaccine responses and faster erosion of vaccine protection, slower wound healing, heightened inflammation, and accelerated cellular aging. Depression also sensitizes immune function, producing larger inflammatory responses when individuals encounter stressors. Loneliness, low support, and distressed relationships can amplify stress reactivity and are linked to greater inflammatory and metabolic vulnerability, including postprandial inflammatory and endothelial responses. More recent work has extended these pathways to the gut microbiome and intestinal permeability (leaky gut), integrating microbial, neuroendocrine, and immune mechanisms. Collectively, the evidence supports a biobehavioral model in which social stress accelerates immune aging and increases risk for inflammation-related disease, while behavioral and nutritional interventions can modify these trajectories.
-
Changes in the Gut Microbiota of Patients After SARS-CoV-2 Infection: What Do We Know?
COVID-19 can cause long-term symptoms, such as a post-infection syndrome, known as Long-COVID. Among the symptoms present during this period, the most reported are gastrointestinal symptoms. This study discusses the effects of changes in the gut microbiota of post-COVID-19 patients. SARS-CoV-2 infection is associated with significant alterations in gut microbial composition, disturbing its homeostasis and promoting a reduction in the abundance of beneficial symbiotic bacteria and an increase in the abundance of opportunistic pathogens. Furthermore, the composition of the gut microbiota may play a role in the prognosis of patients with post-COVID-19 infection. The microbiota of the intestinal tract and the respiratory tract influence each other; therefore, the gut-lung axis has attracted increasing interest in understanding COVID-19. Moreover, the brain-gut axis has been studied, since there have been reports of anxiety and depression along with post-COVID-19 gastrointestinal symptoms. Treatments options for intestinal dysbiosis in Long-COVID patients include probiotics, prebiotics, and fecal microbiota transplantation. These treatments may serve as an approach to improve gastrointestinal symptoms during Long-COVID, increasing microbiome diversity, strengthening the integrity of intestinal barrier functions, and consequently influencing the treatment of COVID-19.