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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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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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Gut microbiota, kynurenine pathway and mental disorders - Review.
The intestine and the gut-associated limphoid tissue constitute the largest immunity organ of the human body. Among several possible tryptophan metabolism routes, the kynurenine pathway can be influenced by the gut microbiota. Disturbances of gut biodiversity may cause increased gut permeability and cause systemic inflammation, also related to central nervous system. Proinflammatory cytokines induce kynurenine pathway enzymes resulting in formation of neuroactive metabolites, which are being associated with several psychiatric disorders. The kynurenine pathway may also be influenced by certain bacteria species directly. The aim of this review is to highlight the current knowledge on the interaction of gut microbiota and the central nervous system with the kynurenine pathway taken into special account. Up to date study results on specific psychiatric disorders such as schizophrenia, bipolar disorder, Alzheimer's disease, autism spectrum disorders, depression and alcoholism are presented. Available evidence suggests that toxicity of kynurenine metabolites may be reduced by adjunction of probiotics which can affect proinflammatory cytokines. Due to their potential for modulation of the kynurenine pathway, gut microbiota pose an interesting target for future therapies.
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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.
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Oleoylethanolamide-producing Lactobacillus paracasei F19 improves metabolic and behavioral disorders by restoring intestinal permeability and microbiota-gut-brain axis in high-fat diet-induced obese male mice.
Metabolic and mood disorders elicited by chronic exposure of high-fat diet (HFD) are often associated with intestinal dysbiosis and persistent low-grade inflammation in the small intestine. This leads to remodeling of the epithelial barrier with disruption of the neuroepithelial circuits that control energy homeostasis by the gut-brain axis. Therefore, therapies that restoreintestinal microbial niche and barrier function are promising candidates to counter peripheral metabolic challenges that affect behaviors controlled by the brain. The endogenous oleoylethanolamine (OEA) was found to shape the intestinal microbiota profile towards a "lean-like phenotype", ameliorating pathological profiles of metabolic diseases. Further, OEA displays beneficial effects in several cognitive paradigms and preserves the epithelial barrier integrity, acting as an intestinal "gate-keeper". Here, we developed an "intestinal OEA factory" for the in-situ and controlled release of OEA by using a probiotic-based delivery system. We engineered the Lactobacillus paracasei F19 (LP) to express the human N-acylphosphatidylethanolamine-preferring phospholipase D (NAPEpld) gene and to produce OEA in response to dietary ultra-low oleate supply. We treated 12-week HFD male mice with oleate-probiotic formulations and assessed their impact on metabolic and behavioral dysfunctions, and microbiota-gut-brain signaling after 8 weeks of treatment. NAPE-expressing LP (pNAPE-LP) led to significant reduced weight loss and improved metabolic dysfunction in HFD-treated mice. Further, a parallel improvement in depressive- and anxiety-like phenotypes was associated with the duodenal barrier function retrieval, the restoration of the Firmicutes/Bacteroidetes ratio, and an increase in beneficial bacteria, such as Lactobacillus, Prevotella, and Parabacteroides. The HFD-driven changes both in the enteric and central nervous system were prevented by pNAPE-LP/oleate treatment. Collectively, our data suggest that these effects were mediated by the oleate-dependent release of OEA by pNAPE-LP since no significant effects were observed in HFD mice treated with the native probiotic alone (pLP). This oleate-regulated delivery system of OEA is a safe and efficient probiotic-based strategy for the treatment of metabolic syndrome and related behavioral disorders.
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The involvement of the gut microbiota in postoperative cognitive dysfunction based on integrated metagenomic and metabolomics analysis.
As the population ages and medical technology advances, anesthesia procedures for elderly patients are becoming more common, leading to an increased prevalence of postoperative cognitive dysfunction. However, the etiology and correlation between the gut microbiota and cognitive dysfunction are poorly understood, and research in this area is limited. In this study, mice with postoperative cognitive dysfunction were found to have reduced levels of fatty acid production and anti-inflammatory flora in the gut, and Bacteroides was associated with increased depression, leading to cognitive dysfunction and depression. Furthermore, more specific microbial species were identified in the disease model, suggesting that modulation of host metabolism through gut microbes may be a potential avenue for preventing postoperative cognitive dysfunction.
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Unveiling the therapeutic potential of the gut microbiota-brain axis: Novel insights and clinical applications in neurological disorders.
Over the last several years, the gut microbiota-brain axis has been the focus of medical study, demonstrating the bidirectional nature of gut and brain communication and the resulting influence on neurological and mental health. Trillions of microorganisms, particularly those found in the gastrointestinal tract, contribute the most to the pathophysiology recovery of organs that are critical to human health, such as digestive processes and metabolism, immune responses, and even cognitive function. Dysbiosis (a disturbance in the microbiome balance) has been identified as one of the risk factors for neuropsychiatric illnesses such as depression, anxiety, autism spectrum disorder, Parkinson's disease, and Alzheimer's disease. Therapeutic strategies aimed at the gut microbiota, such as probiotics, dietary modifications, prebiotics, and fecal microbiota transplantation, will eventually offer ways to alleviate symptoms associated with these disorders by restoring microbial balance, modulating the immune response, and influencing the production of major neurotransmitters. Innovative drug carriers, such as microbially-derived nanoparticles and probiotics that target particular parts of the gut or microbial communities, may improve pharmaceutical treatment efficacy and specificity. The resolution of difficulties such as ethical concerns, unexpected repercussions, and peak performance optimization in a clinical setting is critical for the advancement of this subject.
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Study on gut microbiota and metabolomics in postmenopausal women.
Menopausal syndrome, occurring during the menopausal stage in women, manifests as symptoms stemming from decreased estrogen levels, such as hot flashes, insomnia, mental disorders (anxiety, depression), and osteoporosis. The bulk of studies have indicated alterations in the gut microbiota of those experiencing menopause syndrome compared to healthy women. However, This article focuses on the alterations in gut microbiota in perimenopausal women. Our study utilized 16 s rRNA sequencing to determine the differences in the gut microbiota and metabolites among 44 menopausal syndrome women. The distribution of gut microbiota in postmenopausal women varies based on the level of follicle stimulating hormone, with changes in gut microbiota abundance taking precedence over symptom onset. Fecal metabolites reveal changes in several metabolites, including Amino acid metabolism (Tyrosine, Tryptophan), Lipid metabolism (Alpha linolenic acid metabolism), and other metabolites. Disturbances in lipid metabolism, triggered by hormonal level fluctuations, can contribute to the development of osteoporosis.
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Gut microbiota composition associated with alterations in cardiorespiratory fitness and psychosocial outcomes among breast cancer survivors.
PURPOSE: In this proof-of-concept pilot study, our purpose was to determine correlations between gut microbiota composition and alterations in cardiorespiratory fitness and psychosocial outcomes among post-primary treatment breast cancer survivors (BCS). METHODS: Composition of the gut microbiota in BCS (n = 12) was assessed at baseline (M0) and at the end of 3 months (M3) using Illumina MiSeq DNA Sequencing of the 16S rRNA gene. Gut microbiota composition was analyzed using the QIIME bioinformatics software and represented through diversity metrics and taxa analyses. Cardiorespiratory fitness, fatigue, anxiety, depression, and sleep dysfunction were assessed at M0 and M3 via the submaximal treadmill test, Fatigue Symptom Inventory, Hospital Anxiety and Depression Scale, and Pittsburgh Sleep Quality Index, respectively. RESULTS: Increased fatigue interference in BCS was associated with increased mean within-sample Shannon diversity (organism richness and evenness) (p = 0.009). Weighted UniFrac analysis (shifts in taxa relative abundance) revealed significant differences in between-sample (beta) diversity for changes in fatigue interference (p = 0.01) and anxiety (p = 0.022), with a trend observed for fatigue intensity and sleep dysfunction (p < 0.1). Unweighted UniFrac analysis (shifts in taxa types) found significant beta diversity differences for cardiorespiratory fitness (p = 0.026). Prior to false discovery correction (FDR), changes in fitness, fatigue, anxiety, and sleep dysfunction were associated with the frequency of certain gut bacteria genera (e.g., Faecalibacterium, Prevotella, Bacteroides) (p < 0.05). CONCLUSIONS: Correlations may exist between alterations in gut microbiota composition and longitudinal changes in cardiorespiratory fitness, fatigue, and anxiety in BCS. Further research examining the role of the microbiota-gut-brain axis in exercise-induced effects on psychosocial outcomes in BCS is warranted.
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Gut microbiota manipulation as an epilepsy treatment.
Many studies have documented the important role of the gut microbiota (GM) in the regulation of several central nervous system (CNS) processes through the microbiota-gut-brain (MGB) axis. This latter represents the connection between the CNS, the enteric nervous system, the gut and its microbiota through several ascending and descending pathways. The variation of the GM composition is associated with the pathogenesis and/or progression as well as severity of various neuropsychiatric/neurological diseases such as depression, autism spectrum disorder, multiple sclerosis, Parkinson's, and Alzheimer's diseases. Recently, changes in the bacterial composition of the GM have also been linked to epilepsy and seizures, with some studies exploring the potential role of GM in the regulation of neuronal hyperexcitability, seizure occurrence and epileptogenesis. Accordingly, there are potential novel treatments which are currently being investigated such as probiotics, prebiotics and symbiotic that may represent innovative therapeutic approaches. The aim of this review is to explore the effect of gut microbiota manipulation as a therapeutic strategy in epilepsy and the methodological challenges to design (translational) clinical trial investigating the gut microbiota.