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Early life stress in mice alters gut microbiota independent of maternal microbiota inheritance.
Exposure to early life stress (ELS) is associated with a greater risk of chronic disease development including depression and cardiovascular disease. Altered gut microbiota has been linked to both depression and cardiovascular disease in mice and humans. Rodent models of early life neglect are used to characterize the mechanistic links between early life stress (ELS) and the risk of disease later in life. However, little is understood about ELS exposure and the gut microbiota in the young mice and the influence of the maternal inheritance of the gut microbiota. We used a mouse model of ELS, maternal separation with early weaning (MSEW), and normally reared mice to determine whether the neonate microbiota is altered, and if so, are the differences attributable to changes in dam microbiota that are then transmitted to their offspring. Individual amplicon sequence variants (ASVs) displayed differential abundance in the microbiota of MSEW compared with normally reared pups at postnatal day (PD) 28. Additionally, ELS exposure reduced the alpha diversity and altered microbial community composition at PD28. The composition, levels of alpha diversity, and abundance of individual ASVs in the microbiota of dams were similar from MSEW or normally reared cohorts. Thus, the observed shifts in the abundance of individual bacterial ASVs in the neonates and young pups are likely driven by endogenous effects of MSEW in the offspring host and are not due to inherited differences from the dam. This knowledge suggests that exposure to ELS has a direct effect on microbial factors on the risk of chronic disease development.
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Gut microbiota-derived outer membrane vesicles: under-recognized major players in health and disease?
The role of gut microbiota both in human health and in disease is the subject of intense investigation. The interactions between gut microbiota and the host involve a complex network of metabolic pathways and of biologically active molecules secreted by intestinal bacteria, some of which are packed into nanoparticles known as outer membrane vesicles (OMVs). OMVs can enter the systemic circulation and be delivered to different organs including the brain, eliciting a variety of immunological and metabolic responses. The resulting acute and chronic effects are largely unknown. However, recent studies suggest that OMVs could play a critical role in immune homeostasis and in acute inflammatory reactions. Moreover, the "leaky gut" hypothesis has recently emphasized the role of the brain-gut axis in the pathogenesis of major depressive disorders, pointing to the importance of bacteria and of bacterial products delivered into the circulation in eliciting the low-grade inflammatory response associated with this syndrome. Interestingly, experimental evidence suggests that OMVs can also affect the permeability of the blood-brain barrier. This review also highlights the importance of investigating possible influences of OMVs on the development of the immune system.
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Co-encapsulation of probiotics with functional components: design strategies, synergistic mechanisms, biomedical applications, and challenges for industrialization.
Chronic diseases such as depression, diabetes, inflammatory bowel disease, and colorectal cancer are closely associated with gut microbiota dysbiosis and impaired intestinal barrier function. Probiotic supplementation represents an effective therapeutic approach for modulating gut microecology and alleviating disease symptoms. However, their limited survival rates and colonization efficiency in the gastrointestinal tract compromise their functional efficacy. Co-encapsulation of probiotics with functional components is an effective approach to enhance stability and has gradually become a major focus in current delivery system research. This review summarizes the co-encapsulation strategies of probiotics with functional components, including metabolites, prebiotics, and polyphenols. It also examines the applications of advanced manufacturing technologies such as microfluidics, 3D printing, layer-by-layer encapsulation, and electrospinning/electrospraying in this field. Through functional evaluation methods, including ex vivo gastrointestinal models, in vivo imaging, and metabolic tracking, the advantages of co-encapsulation in improving probiotic survival rates, targeted release capabilities, and functional stability have been demonstrated. Furthermore, this review explores the application potential of co-encapsulation in chronic disease intervention and identifies the challenges that remain in industrial scale-up, safety standardization, and clinical translation. This review aims to provide a scientific foundation for the clinical translation and industrial application of probiotic co-encapsulation technologies.
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Relationships of sleep disturbance, intestinal microbiota, and postoperative pain in breast cancer patients: a prospective observational study.
PURPOSE: Our study was designed to examine the possible relationship between gut microbiota, sleep disturbances, and acute postoperative pain. METHODS: Using 16S rRNA sequencing, we analyzed preoperative fecal samples from women undergoing breast cancer surgery. Preoperative sleep disturbance was evaluated with the Pittsburgh Sleep Quality Index (PSQI) questionnaire. Peak and average pain at rest and movement were evaluated 24 h after surgery, using a numerical rating scale (NRS). Preoperative symptoms of depression and anxiety were assessed with the Patient Health Questionnaire-9 (PHQ-9) and Generalized Anxiety Disorder-7 (GAD-7), respectively. Inflammation was measured using white blood cell and neutrophil counts, together with platelet-lymphocyte ratio, and neutrophil-lymphocyte ratio. RESULTS: Preoperative sleep disturbance was associated with more severe acute postoperative pain. At the phylum level, women with poor sleep quality had higher relative abundance of Firmicutes (p = 0.021) and lower relative abundance of Bacteroidetes (p = 0.013). At the genus level, women with poor sleep quality harbored higher relative abundance of Acidaminococcus and lower relative abundance of several genera. The genus Alloprevotella was negatively associated with peak pain at movement during the first 24 h (r = - 0.592, p < 0.001). The genus Desulfovibrio was negatively associated with symptoms of anxiety (r = - 0.448, p = 0.006). However, partial correlations suggested that the relationship between Alloprevotella and peak pain at movement during the first 24 h was not statistically significant after controlling for sleep (r = - 0.134, p = 0.443). CONCLUSION: These findings suggest that the changed gut microbiota may be involved in sleep-pain interaction and could be applied as a potential preventive method for postoperative pain. TRIAL REGISTRATION: The present clinical study has been registered on Chinese Clinical Trial Registry ( www.chictr.org.cn ); the clinical trial registration number is ChiCTR1900021730; the date of registration is March 7, 2019.
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The Role of the Gut Microbiota in the Metabolism of Polyphenols as Characterized by Gnotobiotic Mice.
A growing body of experimental data suggests that microbes in the gut influence behavior and can alter brain physiology and neurochemistry. Although promising, researchers are only starting to understand the potential of the gut microbiota for use in neurological disease. Recent evidence demonstrated that gastrointestinal activities are linked to mood disorders such as anxiety, depression, and most recently, cognitive functions in age-related neurodegenerative disorders. Studies from our group and others are uncovering new evidence suggesting that the gut microbiota plays a crucial role in the metabolism and bioavailability of certain dietary compounds and synthetic drugs. Based on this evidence, this review article will discuss the implications of the gut microbiota in mechanisms of bioavailability and biotransformation with an emphasis on dietary polyphenol compounds. This will be followed by a survey of ongoing innovative research identifying the ability of individual gut bacteria to enhance the bioavailability of gut-derived, brain-penetrating, bioactive polyphenol metabolites that ultimately influence mechanisms associated with the promotion of resilience against psychological and cognitive impairment in response to stress. Lastly, current research initiatives aimed at promoting the generation of brain bioactive polyphenol metabolites by specialized gut microbes will be discussed, specifically the use of gnotobiotic mice to develop bioengineered second generation probiotics. We propose that leveraging the gut microbial ecosystem to generate brain targeted bioactive metabolites from dietary polyphenols can attenuate lifestyle risk factors and promote resilience against age-related cognitive decline.
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The usefulness of microbiome profiling for geriatric patients with neuropsychiatric conditions: a scoping review.
INTRODUCTION: Neuropsychiatric disorders encompass psychiatric and neurodegenerative diseases. These conditions are particularly challenging to diagnose in the elderly due to their overlapping cognitive, affective, and behavioural symptoms. Recent studies indicate microbiota imbalances exist in both psychiatric and neurodegenerative conditions, suggesting potential biomarkers for diagnosis and prognosis. The objective of this scoping review is to provide a comprehensive overview of how microbiome profiling has been used in research to develop diagnostic and prognostic models for elderly patients with neuropsychiatric conditions. METHODS: Following JBI guidelines, a comprehensive search was conducted across four electronic databases (MEDLINE, PsycINFO, SCOPUS, EMBASE) with strategies developed alongside academic librarians. Two independent reviewers screened titles, abstracts, and full texts based on pre-specified inclusion criteria. Data was extracted focusing on participants, study methods, and key findings. RESULTS: Thirty-one studies employing microbiome-based predictive models were identified, primarily targeting Alzheimer's and Parkinson's diseases, with limited research on psychiatric conditions which was only found for depression and schizophrenia. Most studies used 16S rRNA gene sequencing and machine learning models. Findings highlight the potential of gut microbiota data to enhance predictions of neuropsychiatric conditions, though limitations included small, non-diverse cohorts and a lack of methodological standardisation. The review highlights the need for larger, longitudinal, multicentere studies to validate models and improve clinical applicability. DISCUSSION: Microbiome-based predictive models for neuropsychiatric conditions in the elderly show promise. Future research should focus on longitudinal studies and expanding profiling methods to validate findings in larger, diverse cohorts.
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Effects of Gut Microbiota Alterations on Motor, Gastrointestinal, and Behavioral Phenotype in a Mouse Model of Parkinson's Disease.
BACKGROUND: Parkinson's disease (PD) is a multi-system disorder consisting of not only classic motor symptoms but also a variety of non-motor symptoms including gastrointestinal (GI) dysfunction and mood disorders. The gut microbiota has been suggested to play a role in modulating PD motor and non-motor features, although the causality and mechanisms behind these proposed interactions remains largely understudied. OBJECTIVE: In this study, we aimed to provide in-depth characterization of an established mouse model of PD (transgenic (TG) SNCA A53T) and experimentally address how changes to the gut microbiota impact the PD-like phenotype. METHODS: We profiled the PD-like phenotype of transgenic mice through a panel of motor, GI, and behavioral tests. We then investigated how antibiotic treatment or gut microbial community transfer (via cohousing with wild-type mice) impacted the PD-like phenotype. RESULTS: We found that this mouse model demonstrated early (6 weeks of age) motor symptoms when compared to a wild-type control mouse strain. Transgenic mice also exhibited early GI dysfunction, as well as behavioral alterations, including reduced anxiety-like behavior, and increased depression-like and apathy-like behavior. Compared to wild-type mice, the transgenic fecal microbiota was less diverse and compositionally distinct. Interestingly, drastic alterations to the gut microbiota, through antibiotic treatment or cohousing with wild-type mice, had a minimal effect on the motor, GI, and behavioral phenotype of transgenic mice. CONCLUSION: We concluded that this mouse model effectively recapitulates motor and non-motor features of PD; however, the gut microbiota appears to exhibit a minor impact on the pathophysiology of this PD model.
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ASMT determines gut microbiota and increases neurobehavioral adaptability to exercise in female mice.
N-acetylserotonin O-methyltransferase (ASMT) is responsible for melatonin biosynthesis. The Asmt gene is located on the X chromosome, and its genetic polymorphism is associated with depression in humans. However, the underlying mechanism remains unclear. Here, we use CRISPR/Cas9 to delete 20 bp of exon 2 of Asmt, and construct C57BL/6J mouse strain with Asmt frameshift mutation (Asmtft/ft). We show that female Asmtft/ft mice exhibit anxiety- and depression-like behaviors, accompanied by an obvious structural remodeling of gut microbiota. These behavioral abnormalities are not observed in male. Moreover, female Asmtft/ft mice show a lower neurobehavioral adaptability to exercise, while wild-type shows a "higher resilience". Cross-sectional and longitudinal analysis indicates that the structure of gut microbiota in Asmtft/ft mice is less affected by exercise. These results suggests that Asmt maintains the plasticity of gut microbiota in female, thereby enhancing the neurobehavioral adaptability to exercise.
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Effects of gut microbiota disturbance induced in early life on the expression of extrasynaptic GABA-A receptor α5 and δ subunits in the hippocampus of adult rats.
Previous studies have demonstrated that gut microbiota disturbance significantly increases the risk of emotional disorders via the gut-brain axis, but the mechanism is unclear. Furthermore, gamma-aminobutyric acid (GABA) deficits were reported to be implicated in the development of depression and amnesia, but the alterations in the GABA-A receptor subunits that are involved in the pathogenetic process have not been fully elucidated. This study used juvenile rats that were fed ampicillin-Na to establish degree III dysbiosis of the intestinal flora and examined emotional change via the tail suspension test, forced swim test and Morris water maze. Additionally, our study investigated the expression of GABA-A receptor α5 and δ subunits in the hippocampus in adulthood via q-PCR and immunohistochemistry. We focused on the role of GABA-A receptor α5 and δ subunit changes induced by juvenile gut microbiota disturbance in the pathogenesis of emotional disorders in adulthood. In addition, we investigated the protective effects of probiotics and benzodiazepine (clonazepam). Findings showed that juvenile gut microbiota disturbances induced chronic depression and memory loss and reduced the expression of GABA-A receptor α5 and δ subunits in the hippocampus of the adult rat. Furthermore, moderate probiotic administration led to a significant improvement compared to short-term BZ treatment. However, we are aware that these results have been established with a single animal experiment and will require further confirmation with a larger group of individuals. Future directions for the exploration of the effects of gut microbiota disturbance on GABA-A receptor α5 and δ subunits are discussed.
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Perturbations in the microbiota-gut-brain axis shaped by social status loss.
Social status is closely linked to physiological and psychological states. Loss of social dominance can lead to brain disorders such as depression, but the underlying mechanisms remain unclear. The gut microbiota can sense stress and contribute to brain disorders via the microbiota-gut-brain axis (MGBA). Here, using a forced loss paradigm to demote dominant mice to subordinate ranks, we find that stress alters the composition and function of the gut microbiota, increasing Muribaculaceae abundance and enhancing butanoate metabolism, and gut microbial depletion resists forced loss-induced hierarchical demotion and behavioral alteration. Single-nucleus transcriptomic analysis of the prefrontal cortex (PFC) indicates that social status loss primarily affected interneurons, altering GABAergic synaptic transmission. Weighted gene co-expression network analysis (WGCNA) reveals modules linked to forced loss in the gut microbiota, colon, PFC, and PFC interneurons, suggesting changes in the PI3K-Akt signaling pathway and the glutamatergic synapse. Our findings provide evidence for MGBA perturbations induced by social status loss, offering potential intervention targets for related brain disorders.