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Gut Microbiota and Ischemic Stroke: From Pre-Stroke Dysbiosis and Acute-Phase Changes to Therapeutic Applications.
PURPOSE: Ischemic stroke poses a major global health burden, and growing evidence points to the microbiota-gut-brain axis as an important contributor to stroke pathophysiology and recovery. The purpose of this review is to summarize current knowledge on bidirectional gut-brain communication in stroke, establishing gut dysbiosis as an upstream risk factor for stroke onset and examining microbiota dynamics across acute and chronic phases. METHOD: A comprehensive review of the current literature was conducted to synthesize existing evidence on the mechanisms of gut-brain communication, the influence of host factors, post-stroke complications, and candidate therapeutic interventions targeting the MGBA in ischemic stroke. FINDING: Gut dysbiosis acts as a risk factor for stroke through TMAO-mediated atherothrombosis, systemic inflammatory priming, and comorbidity-associated dysbiotic pre-conditioning. Following a stroke, dysbiosis is characterized by a depletion of short-chain fatty acid (SCFA)-producing taxa and an expansion of pro-inflammatory bacteria, particularly Proteobacteria and Enterobacteriaceae. Host factors (age, sex, genetics, and comorbidities) shape microbiota signatures and influence outcomes. Furthermore, post-stroke complications-including cognitive impairment, depression, stroke-associated pneumonia, and gastrointestinal dysfunction-are intimately linked to persistent dysbiosis. Mechanistically, the gut microbiota modulates stroke outcomes through immune regulation, metabolite signaling, blood-brain barrier integrity, and vagal pathways. Candidate therapeutic interventions (probiotics/prebiotics, fecal microbiota transplantation, SCFA supplementation, traditional Chinese medicine, and neuromodulation) demonstrate promising neuroprotective and recovery-enhancing effects, predominantly in preclinical models. CONCLUSION: While targeted interventions like probiotics and dietary fiber supplementation have shown modest benefits in small clinical trials, human clinical evidence remains largely preliminary. The translation of FMT, SCFA supplementation, and neuromodulatory approaches to clinical practice requires validation through rigorous, adequately powered randomized controlled trials. Future precision microbiome medicine demands individualized profiling and phenotype-specific interventions to establish microbiota-targeted strategies as viable adjunctive stroke therapies.
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From Gut to Brain: The roles of intestinal microbiota, immune system, and hormones in intestinal physiology and gut-brain-axis.
The intestine plays numerous roles in the normal physiology of our body. Gut-brain axis (GBA) is a complex communication network linking the gastrointestinal (GI) tract and central nervous system (CNS). This bidirectional system integrates endocrine, neural, and immune signals, impacting host metabolism and cognition. The gut microbiota, a critical component of the GBA, significantly impacts gut hormones, neurotransmission, neural development, and other components of gut-brain-axis. The microbiota-gut-brain axis facilitates communication via metabolites such as short chain fatty acids (SCFAs), and neurotransmitters such as dopamine, γ-amino butyric acid (GABA) and serotonin. The microbiota influences gut peptide production, including ghrelin, glucagon like pepetide-1 (GLP-1), serotonin, and cholecystokinin (CCK), thereby modulating nutrient absorption and immune responses. Gut hormones such as ghrelin, CCK, GLP-1, gastric inhibitory peptide (GIP), serotonin (5-HT), neurotensin, peptide YY (PYY) and melatonin play key roles in the GBA. These hormones play several roles including modulation of appetite and satiety, metabolism of nutrients such as lipid and glucose, insulin and glucagon secretion, and influence on gut inflammation, mood, learning and cognition. The interaction between gut microbiota and these hormones underscores their role in maintaining gut-brain homeostasis. Dysbiosis, or microbial imbalance, is linked to altered stress responses, anxiety, and depressive behaviors, highlighting the therapeutic potential of microbiota modulation. Despite the significant roles of gut hormones and microbiota in the GBA, literature on their cellular and molecular mechanisms is limited, and often based on animal models. This review synthesizes current understanding of hormones secreted by the intestine, their physiological effects and the cellular and molecular mechanisms of action underlying these effects, with a focus on their roles in the GBA. By elucidating these complex relationships, the review aims to advance research and clinical applications, offering insights into gastrointestinal and systemic health.
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Interactions between gut microbiota, plasma metabolome and brain function in the setting of a HIV cure trial.
BACKGROUND: The intestinal microbiota composition has been linked to neurocognitive impairment in people with HIV (PWH). However, the potential interplay of microbial species and related metabolites, particularly in the context of an HIV cure strategy remains underexplored. The BCN02 trial evaluated the impact of romidepsin (RMD), used as a HIV-1 latency reversing agent and with reported beneficial neurological effects, combined with the MVA.HIVconsv vaccine on virus control during 32-weeks of monitored antiretroviral treatment interruption (MAP) in early-treated HIV-infected individuals. Here, we analyzed longitudinal gut microbiome, plasma metabolome and brain functioning data to identify potential associations and novel putative biomarkers of HIV-associated neurocognitive disorders (HAND). METHODS: Data from fecal shotgun metagenomics, plasma metabolome, cognitive (standardized neuropsychological test score covering 6 cognitive domains, NPZ-6), functional (neuropsychiatric symptoms) and neuroimaging assessments were obtained and evaluated in 18 participants before and after RMD administration, and at the study end (post-MAP follow-up) in the BCN02 trial. RESULTS: Participants with neurocognitive impairment (Lower vs. Higher NPZ-6 score group) were enriched in bacterial species, including Desulfovibrio desulfuricans, Sutterella wadsworthensis and Streptococcus thermophilus, and showed higher 1,2-propanediol degradation microbial pathway levels, before RMD administration. A multi-omics profiling showed significant and positive correlations between these microbial features and lipid-related metabolic pathways, previously linked to neurological disorders (i.e., sphingolipid, ether lipid, and glycerophospholipid metabolism), in participants with neurocognitive impairment, before RMD administration. Three indices (microbial-, metabolite-based and combined) obtained from the discriminant features were assessed longitudinally, showing progressive similarities between NPZ-6 score groups over time. Furthermore, the three indices and related discriminant features correlated negatively with functional outcomes, such as quality of life and daily functioning, and positively with depression, stress and CNS-related symptoms before RMD administration, while these associations became less discernible at the subsequent timepoints. CONCLUSIONS: While the direct effect of the intervention on the observed shifts cannot be conclusively determined in this study settings, these findings strengthen the link between gut bacteria, related metabolites, and neurocognitive function in PWH, and provide an analytical framework for future validation studies aimed at discovering predictive biomarkers for neurocognitive impairment in PWH.
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Gut bacteriome and mood disorders in women with PCOS.
STUDY QUESTION: How does the gut bacteriome differ based on mood disorders (MDs) in women with polycystic ovary syndrome (PCOS), and how can the gut bacteriome contribute to the associations between these two conditions? SUMMARY ANSWER: Women with PCOS who also have MDs exhibited a distinct gut bacteriome with reduced alpha diversity and a significantly lower abundance of Butyricicoccus compared to women with PCOS but without MDs. WHAT IS KNOWN ALREADY: Women with PCOS have a 4- to 5-fold higher risk of having MDs compared to women without PCOS. The gut bacteriome has been suggested to influence the pathophysiology of both PCOS and MDs. STUDY DESIGN, SIZE, DURATION: This population-based cohort study was derived from the Northern Finland Birth Cohort 1966 (NFBC1966), which includes all women born in Northern Finland in 1966. Women with PCOS who donated a stool sample at age 46 years (n = 102) and two BMI-matched controls for each case (n = 205), who also responded properly to the MD criteria scales, were included. PARTICIPANTS/MATERIALS, SETTING, METHODS: A total of 102 women with PCOS and 205 age- and BMI-matched women without PCOS were included. Based on the validated MD criteria, the subjects were categorized into MD or no-MD groups, resulting in the following subgroups: PCOS no-MD (n = 84), PCOS MD (n = 18), control no-MD (n = 180), and control MD (n = 25). Clinical characteristics were assessed at age 31 years and age 46 years, and stool samples were collected from the women at age 46 years, followed by the gut bacteriome analysis using 16 s rRNA sequencing. Alpha diversity was assessed using observed features and Shannon's index, with a focus on genera, and beta diversity was characterized using principal components analysis (PCA) with Bray-Curtis Dissimilarity at the genus level. Associations between the gut bacteriome and PCOS-related clinical features were explored by Spearman's correlation coefficient. A P-value for multiple testing was adjusted with the Benjamini-Hochberg false discovery rate (FDR) method. MAIN RESULTS AND THE ROLE OF CHANCE: We observed changes in the gut bacteriome associated with MDs, irrespective of whether the women also had PCOS. Similarly, PCOS MD cases showed a lower alpha diversity (Observed feature, PCOS no-MD, median 272; PCOS MD, median 208, FDR = 0.01; Shannon, PCOS no-MD, median 5.95; PCOS MD, median 5.57, FDR = 0.01) but also a lower abundance of Butyricicoccus (log-fold changeAnalysis of Compositions of Microbiomes with Bias Correction (ANCOM-BC)=-0.90, FDRANCOM-BC=0.04) compared to PCOS no-MD cases. In contrast, in the controls, the gut bacteriome did not differ based on MDs. Furthermore, in the PCOS group, Sutterella showed positive correlations with PCOS-related clinical parameters linked to obesity (BMI, r2=0.31, FDR = 0.01; waist circumference, r2=0.29, FDR = 0.02), glucose metabolism (fasting glucose, r2=0.46, FDR < 0.001; fasting insulin, r2=0.24, FDR = 0.05), and gut barrier integrity (zonulin, r2=0.25, FDR = 0.03). LIMITATIONS, REASONS FOR CAUTION: Although this was the first study to assess the link between the gut bacteriome and MDs in PCOS and included the largest PCOS dataset for the gut microbiome analysis, the number of subjects stratified by the presence of MDs was limited when contrasted with previous studies that focused on MDs in a non-selected population. WIDER IMPLICATIONS OF THE FINDINGS: The main finding is that gut bacteriome is associated with MDs irrespective of the PCOS status, but PCOS may also modulate further the connection between the gut bacteriome and MDs. STUDY FUNDING/COMPETING INTEREST(S): This research was funded by the European Union's Horizon 2020 Research and Innovation Programme under the Marie Sklodowska-Curie Grant Agreement (MATER, No. 813707), the Academy of Finland (project grants 315921, 321763, 336449), the Sigrid Jusélius Foundation, Novo Nordisk Foundation (NNF21OC0070372), grant numbers PID2021-12728OB-100 (Endo-Map) and CNS2022-135999 (ROSY) funded by MCIN/AEI/10.13039/501100011033 and ERFD A Way of Making Europe. The study was also supported by EU QLG1-CT-2000-01643 (EUROBLCS) (E51560), NorFA (731, 20056, 30167), USA/NIH 2000 G DF682 (50945), the Estonian Research Council (PRG1076, PRG1414), EMBO Installation (3573), and Horizon 2020 Innovation Grant (ERIN, No. EU952516). The funders did not participate in any process of the study. We have no conflicts of interest to declare. TRIAL REGISTRATION NUMBER: N/A.
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Stress and the gut microbiota-brain axis.
The gut microbiota-brain axis is a complex system that links the bacteria in our gut with our brain, it plays a part in what way we respond to stress. This chapter explores how stress affects the types of bacteria in the gut and shows the two-way connection between them. Stress can change the bacteria in our gut, which can cause various problems related to stress, like depression, anxiety, and irritable bowel syndrome (IBS). Figuring out how these interactions may help us develop new treatments that focus on the connection between gut bacteria and the brain. This chapter looks at how gut bacteria could help identify stress-related problems. It also discusses the difficulties and possibilities of using this research in medical practice. In the end, the chapter talks about what comes next in this quickly changing area. It highlights how important it is to include research about the gut-brain connection in overall public health plans.
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Electro-microbial interplay in the gut-brain axis: An emerging paradigm for gut microbiota modulation via vagus nerve stimulation.
The treatment of central nervous system disorders remains a clinical challenge, highlighting an urgent need for innovative therapeutic strategies. The gut-brain axis represents a complex bidirectional communication network between the gastrointestinal tract and the brain, with the vagus nerve serving as a critical pathway for signal transmission. Vagus nerve stimulation (VNS), an established therapy for drug-resistant epilepsy and depression, has been shown to modulate the composition and functional output of gut microbiota, which in turn influences disease progression. Concurrently, gut microbiota and their metabolites such as short-chain fatty acids can regulate vagal activity through feedback mechanisms. This bidirectional interaction operates through neural, immune and metabolic pathways. This review provides a systematic review of the mechanisms through which VNS influences gut microbiota, and how microbial products feedback to regulate vagus nerve activity and the integrated pathways underlying this cross-talk, for the sake of providing insights into novel therapeutic approaches targeting the gut-brain interface.
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Risk factors for developing irritable bowel syndrome: systematic umbrella review of reviews.
BACKGROUND: Irritable bowel syndrome (IBS) is a debilitating disorder affecting 4-9% of the global population. It is a multifaceted disorder with complex and varied causes. This review aims to consolidate the evidence regarding IBS risk factors by examining existing systematic reviews and meta-analyses, covering potential genetic, immunological, psychological, and dietary causes. METHODS: Systematic literature searches were conducted in MEDLINE, Embase and Cochrane library databases. Study selection and data extraction were conducted independently by four authors, with discrepancies resolved by consensus with a senior author. Systematic reviews examining risk factors of IBS development were eligible for review. Results were narratively synthesized. Quality of reviews were analysed using AMSTAR 2, and evidence were appraised using GRADE methodology. RESULTS: A total of 69 systematic reviews were included in this study. Most reviews were of "critically low" quality, while the remaining were "low" quality. Common shortcomings included the absence of a list of excluded studies with justifications for their exclusion and inadequate consideration of the risk of bias in individual studies. Eight major categories of risk factors for IBS identified were as follows: dietary, genetic, environmental, psychological, gut microbiome, socio-economic, physiological, and pathological, albeit overlaps exist. The most frequently reported risk factors for IBS development were female gender and anxiety disorders, with overall GRADE evaluation of "low"; depression and gastroenteritis, with overall GRADE evaluation of "moderate". CONCLUSIONS: Clinical practice should prioritize recognition of these risk factors. Future reviews should improve their reporting of results based on the PRISMA guidelines, to enhance the quality of research in this field. PROTOCOL REGISTRATION: PROSPERO CRD42023493739.
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The Effects of Stress and Meditation on the Immune System, Human Microbiota, and Epigenetics.
Context • Globally, more than 25% of individuals are affected by anxiety and depression disorders. Meditation is gaining popularity in clinical settings and its treatment efficacy is being studied for a wide array of psychological and physiological ailments. An exploration of stress physiology is an essential precursor to delineation of the mechanisms underlying the beneficial effects of meditation practices. Objective • The review outlines a model of interconnected physiological processes that might support the continued inclusion and expansion of meditation in the treatment of diverse medical conditions and to investigate the role that gut microbiota may play in realizing well-being through meditation. Design • The authors conducted a scientific literature database search with the goal of reviewing the link between stress management techniques and human microbiota. Their goal was also to identify the extent of underlying epigenetic reactions in these processes. The review was completed in approximately 2 y. Databases searched included Medline via PubMed and Ovid, PsycINFO via Ovid, Spinet, ProQuest Central, SAGE Research Methods Online, CINAHL Plus with Full Text, Science Direct, Springer Link, and Wiley Online Library. Keywords searched included, but were not limited to, stress, meditation, mindfulness, immune system, HPA axis, sympathetic nervous system, parasympathetic nervous system, microbiota, microbiome, gut-barrier function, leaky gut, vagus nerve, psychoneuroimmunology, epigenetic, and NF-κB. Setting • The study took place at New York University (New York, NY, USA), the University of California, San Diego (La Jolla, CA, USA), and the Chopra Foundation (Carlsbad, CA, USA). Results • Psychological stress typically triggers a fight-or-flight response, prompting corticotropin-releasing hormone and catecholamine production in various parts of the body, which ultimately disturbs the microbiota. In the absence of stress, a healthy microbiota produces short-chain fatty acids that exert anti-inflammatory and antitumor effects. During stress, an altered gut microbial population affects the regulation of neurotransmitters mediated by the microbiome and gut barrier function. Meditation helps regulate the stress response, thereby suppressing chronic inflammation states and maintaining a healthy gut-barrier function. Conclusions • The current research team recommends the integration of meditation into conventional health care and wellness models. Concurrently, studies to explore the effects of meditation on human microbiota are warranted.
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Strain differences in the susceptibility to the gut-brain axis and neurobehavioural alterations induced by maternal immune activation in mice.
There is a growing realization that the severity of the core symptoms of autism spectrum disorders and schizophrenia is associated with gastrointestinal dysfunction. Nonetheless, the mechanisms underlying such comorbidities remain unknown. Several genetic and environmental factors have been linked to a higher susceptibility to neurodevelopmental abnormalities. The maternal immune activation (MIA) rodent model is a valuable tool for elucidating the basis of this interaction. We induced MIA with polyinosinic-polycytidylic acid (poly I:C) at gestational day 12.5 and assessed behavioural, physiological and molecular aspects relevant to the gut-brain axis in the offspring of an outbred (NIH Swiss) and an inbred (C57BL6/J) mouse strain. Our results showed that the specific MIA protocol employed induces social deficits in both strains. However, alterations in anxiety and depression-like behaviours were more pronounced in NIH Swiss mice. These strain-specific behavioural effects in the NIH Swiss mice were associated with marked changes in important components of gut-brain axis communication: the endocrine response to stress and gut permeability. In addition, MIA-induced changes in vasopressin receptor 1a mRNA expression in the hypothalamus were observed in NIH Swiss mice only. Taken together, these data suggest that genetic background is a critical factor in susceptibility to the gut-brain axis effects induced by MIA.
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Ideal dietary fiber model: Personalized gut microbiota modulation based on structure-function relationships.
Dietary fiber has emerged as a central modulator of gut microbiota composition and host physiology, garnering unprecedented scientific attention. Here, we propose the "Ideal Dietary Fiber Model"-a personalized, structure-guided framework designed to precisely shape gut microbial ecosystems and promote host health. Departing from traditional fiber classifications, this model emphasizes the construction of composite fiber formulations based on detailed structural parameters, including monosaccharide composition, glycosidic linkage types, and degree of polymerization. Particular focus is given to oligosaccharides, whose fine structural features confer high selectivity in modulating microbial communities and the production of key metabolites such as short-chain fatty acids, indoles, and neurotransmitter precursors. This review synthesizes recent advances in fiber-microbiota interactions across metabolic, inflammatory, and neurocognitive diseases, including obesity, type 2 diabetes, Non-Alcoholic Fatty Liver Disease, inflammatory bowel disease, colorectal cancer, depression, anxiety, and Alzheimer's disease. While mechanistic insights continue to expand, current evidence remains largely preclinical, highlighting the gap between experimental findings and clinical translation. We argue that integrating microbiome stratification with fiber structure-function databases will be essential for advancing precision nutrition. The Ideal Dietary Fiber Model offers a conceptual and practical foundation for microbiota-targeted dietary design, but its therapeutic potential requires rigorous clinical validation.