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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.
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Insights on the Critical Parameters Affecting the Probiotic Viability During Stabilization Process and Formulation Development.
Probiotics have gained a lot of interest in recent years as an alternative as well as adjuvant therapy for several conditions owing to their health benefits. These live microorganisms have proven efficacy for treating gut disorders, inflammation, bacterial vaginosis, hepatic and depressive disorders, and many more. There are conventional as well as non-conventional formulations available for the delivery of probiotics with the latter having fewer regulatory guidelines. The conventional formulations include the pharmaceutical formulations specifically designed to deliver an efficacious number of viable microorganisms. Studies have indicated 108-109 CFU/g as an ideal dose of probiotics for achieving health benefits, and hence, all the formulations must at least contain the said number of viable bacteria to show a therapeutic effect. The most crucial feature of probiotic formulations is that the bacteria are prone to several environmental and processing factors which all together reduce the viability of the bacteria in the final formulation. These factors include processing parameters like temperature, humidity, pressure, and storage conditions. Thus, the present review primarily focuses on the critical process parameters affecting the probiotic viability during stabilization process and formulation development. Understanding these factors prior to processing helps in delivering probiotics in the required therapeutic numbers at the target site.
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Neural regulation of gut inflammation via autonomic nerves: therapeutic implications for inflammatory bowel disease.
Inflammatory bowel disease (IBD) is a debilitating and treatment-refractory condition with a complex and incompletely understood etiology. Recent advances in neuroimmunology have revealed that intestinal homeostasis is regulated by bidirectional communication between the autonomic nervous system and the immune system. In particular, vagus nerve-mediated cholinergic anti-inflammatory signaling plays a central role in modulating intestinal immune responses and represents a key mechanism linking neural regulation to IBD pathogenesis and therapy. In parallel, the gut-brain axis has emerged as a critical regulator of intestinal inflammation and systemic disease. Psychological stress alters gut immune function through mechanisms involving enteric glial activation and microbiota-derived metabolites, contributing to treatment-resistant depression via immune activation and changes in short-chain fatty acid profiles. Moreover, gut microbiota dysbiosis has been implicated in neurodegenerative disorders such as Alzheimer's and Parkinson's diseases, potentially preceding central pathology through vagal signaling and systemic inflammation. Together, these findings position the gut microbiota as an immunological and neurological hub connecting intestinal, systemic, and brain health. This review summarizes recent advances in gut-brain axis-mediated immune regulation in IBD and highlights emerging bioelectronic neuromodulation strategies targeting autonomic circuits as promising non-pharmacological approaches to restore gut immune balance.
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Cognition and gut microbiota in schizophrenia spectrum and mood disorders: A systematic review.
FRILEUX, M., BOLTRI M. and al. Cognition and Gut microbiota in schizophrenia spectrum and mood disorders: a Systematic Review. NEUROSCI BIOBEHAV REV (1) 2024 Schizophrenia spectrum disorders and major mood disorders are associated with cognitive impairments. Recent studies suggest a link between gut microbiota composition and cognitive functioning. Here, we review the relationship between gut microbiota and cognition in these disorders. To do this, we conducted a systematic review, searching Cochrane Central Register of Controlled Trials, EBSCOhost, Embase, Pubmed, Scopus, and Web of Science. Studies were included if they investigated the relationship between gut microbiota composition and cognitive function through neuropsychological assessments in patients with bipolar, depressive, schizophrenia spectrum, and other psychotic disorders. Ten studies were identified. Findings underscore a link between gut dysbiosis and cognitive impairment. This relationship identified specific taxa (Haemophilus, Bacteroides, and Alistipes) as potential contributors to bolstered cognitive performance. Conversely, Candida albicans, Toxoplasma gondii, Streptococcus and Deinococcus were associated with diminished performance on cognitive assessments. Prebiotics and probiotics interventions were associated with cognitive enhancements, particularly executive functions. These results emphasize the role of gut microbiota in cognition, prompting further exploration of the underlying mechanisms paving the way toward precision psychiatry.
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Blood metabolomic profiling reveals new targets in the management of psychological symptoms associated with severe alcohol use disorder.
BACKGROUND: Alcohol use disorder (AUD) is a global health problem with limited therapeutic options. The biochemical mechanisms that lead to this disorder are not yet fully understood, and in this respect, metabolomics represents a promising approach to decipher metabolic events related to AUD. The plasma metabolome contains a plethora of bioactive molecules that reflects the functional changes in host metabolism but also the impact of the gut microbiome and nutritional habits. METHODS: In this study, we investigated the impact of severe AUD (sAUD), and of a 3-week period of alcohol abstinence, on the blood metabolome (non-targeted LC-MS metabolomics analysis) in 96 sAUD patients hospitalized for alcohol withdrawal. RESULTS: We found that the plasma levels of different lipids ((lyso)phosphatidylcholines, long-chain fatty acids), short-chain fatty acids (i.e. 3-hydroxyvaleric acid) and bile acids were altered in sAUD patients. In addition, several microbial metabolites, including indole-3-propionic acid, p-cresol sulfate, hippuric acid, pyrocatechol sulfate, and metabolites belonging to xanthine class (paraxanthine, theobromine and theophylline) were sensitive to alcohol exposure and alcohol withdrawal. 3-Hydroxyvaleric acid, caffeine metabolites (theobromine, paraxanthine, and theophylline) and microbial metabolites (hippuric acid and pyrocatechol sulfate) were correlated with anxiety, depression and alcohol craving. Metabolomics analysis in postmortem samples of frontal cortex and cerebrospinal fluid of those consuming a high level of alcohol revealed that those metabolites can be found also in brain tissue. CONCLUSIONS: Our data allow the identification of neuroactive metabolites, from interactions between food components and microbiota, which may represent new targets arising in the management of neuropsychiatric diseases such as sAUD. FUNDING: Gut2Behave project was initiated from ERA-NET NEURON network (Joint Transnational Call 2019) and was financed by Academy of Finland, French National Research Agency (ANR-19-NEUR-0003-03) and the Fonds de la Recherche Scientifique (FRS-FNRS; PINT-MULTI R.8013.19, Belgium). Metabolomics analysis of the TSDS samples was supported by grant from the Finnish Foundation for Alcohol Studies.
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Effects of dietary FODMAP content on the faecal microbiome and gastrointestinal physiology in healthy adults: a randomised, controlled cross-over feeding study.
The effect of dietary FODMAP (fermentable oligo-, di- and mono-saccharides and polyols) in healthy adults is poorly documented. This study compared the specific effects of low and moderate FODMAP intake (relative to typical intake) on the faecal microbiome, participant-reported outcomes and gastrointestinal physiology. In a single-blind cross-over study, twenty-five healthy participants were randomised to one of two provided diets, 'low' (LFD) <4 g/d or 'moderate' (MFD) 14-18 g/d, for 3 weeks each, with ≥ 2-week washout between. Endpoints were assessed in the last week of each diet. The faecal bacterial/archaeal and fungal communities were characterised by eighteen participants from whom high-quality DNA was extracted by 16S rRNA and internal transcribed spacer 2 (ITS2) profiling and metagenomic sequencing. There were no differences in gastrointestinal or behavioural symptoms (fatigue, depression, anxiety) or faecal characteristics and biochemistry (including SCFA). Mean colonic transit time (telemetry) was 23 (95 % CI: 15, 30) h with the MFD compared with 34 (24, 44) h with LFD (n 12; P = 0·009). Fungal diversity (richness) increased in response to MFD, but the bacterial richness was reduced, coincident with the expansion of the relative abundances of Bifidobacterium, Anaerostipes and Eubacterium. Metagenomic analysis showed expansion of polyol-utilising Bifidobacteria and Anaerostipes with MFD. In conclusion, short-term alterations of FODMAP intake are not associated with symptomatic, stool or behavioural manifestations in healthy adults, but remarkable shifts within the bacterial and mycobiome populations were observed. These findings emphasise the need to quantitatively assess all microbial domains and their interrelationships to improve understanding of the consequences of diet on gut function.
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The role of the indoles in microbiota-gut-brain axis and potential therapeutic targets: A focus on human neurological and neuropsychiatric diseases.
At present, a large number of relevant studies have suggested that the changes in gut microbiota are related to the course of nervous system diseases, and the microbiota-gut-brain axis is necessary for the proper functioning of the nervous system. Indole and its derivatives, as the products of the gut microbiota metabolism of tryptophan, can be used as ligands to regulate inflammation and autoimmune response in vivo. In recent years, some studies have found that the levels of indole and its derivatives differ significantly between patients with central nervous system diseases and healthy individuals, suggesting that they may be important mediators for the involvement of the microbiota-gut-brain axis in the disease course. Tryptophan metabolites produced by gut microbiota are involved in multiple physiological reactions, take indole for example, it participates in the process of inflammation and anti-inflammatory effects through various cellular physiological activities mediated by aromatic hydrocarbon receptors (AHR), which can influence a variety of neurological and neuropsychiatric diseases. This review mainly explores and summarizes the relationship between indoles and human neurological and neuropsychiatric disorders, including ischemic stroke, Alzheimer's disease, Parkinson's disease, multiple sclerosis, cognitive impairment, depression and anxiety, and puts forward that the level of indoles can be regulated through various direct or indirect ways to improve the prognosis of central nervous system diseases and reverse the dysfunction of the microbiota-gut-brain axis. This article is part of the Special Issue on "Microbiome & the Brain: Mechanisms & Maladies".
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Could psychobiotics and fermented foods improve mood in middle-aged and older women?
Menopause is a natural physiological phase during which women experience dramatic hormonal fluctuations. These lead to many symptoms, such as depression and anxiety, which, in turn, can negatively affect quality of life. Proper nutrition has an influential role in alleviating depression as well as anxiety. It is well known that gut microbiota dysbiosis contributes to the development of mood disorder. There is mounting evidence that modulating the gut-brain axis may aid in improving mood swings. In this context, this narrative review summarizes recent findings on how aging changes the composition of the gut microbiota and on the association between gut microbiota and mood disorders. In addition, it evaluates the effectiveness of psychobiotics and fermented foods in treating mood swings in middle-aged and older women. A search was done using PubMed, Scopus, and Google Scholar, and thirteen recent articles are included in this review. It is evident that psychobiotic supplementation and fermented foods can improve mood swings via several routes. However, these conclusions are based on only a few studies in middle-aged and older women. Therefore, long-term, well-designed randomized controlled trials are required to fully evaluate whether psychobiotics and fermented foods can be used to treat mood swings in this population.
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Long-Term Exposure to Ceftriaxone Sodium Induces Alteration of Gut Microbiota Accompanied by Abnormal Behaviors in Mice.
Background: Growing evidence points out that a disturbance of gut microbiota may also disturb the gut-brain communication. However, it is not clear to what extent the alteration of microbiota composition can modulate brain function, affecting host behaviors. Here, we investigated the effects of gut microbiota depletion on emotional behaviors. Methods: Mice in the experimental group were orally administered ceftriaxone sodium solution (250 mg/ml, 0.2 ml/d) for 11 weeks. The open-field test and tail-suspension test were employed for the neurobehavioral assessment of the mice. Fecal samples were collected for 16s rDNA sequencing. The serum levels of cytokines and corticosterone were quantified using enzyme-linked immunosorbent assays. The immunohistochemistry method was used for the detection of brain-derived neurotrophic factor (BDNF) and c-Fos protein. Results: The gut microbiota for antibiotic-treated mice showed lower richness and diversity compared with normal controls. This effect was accompanied by increased anxiety-like, depression-like, and aggressive behaviors. We found these changes to be possibly associated with a dysregulation of the immune system, abnormal activity of the hypothalamic-pituitary-adrenal axis, and an alteration of neurochemistry. Conclusions: The findings demonstrate the indispensable role of microbiota in the gut-brain communication and suggest that the absence of conventional gut microbiota could affect the nervous system, influencing brain function.
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Microbial regulation of a lincRNA-miRNA-mRNA network in the mouse hippocampus.
Aim: To comprehensively understand microbiota-regulated lincRNA-miRNA-mRNA networks in psychiatric disorders. Materials & methods: Integrated analyses of lincRNAs, mRNAs and miRNAs, obtained by microarray analysis of hippocampus from specific pathogen-free, germ-free and colonized germ-free mice, were performed. Results: Expression of 139 mRNAs, seven miRNAs and one lincRNA was restored following colonization. The restored transcripts were mainly involved in CREB and Ras/MAPK signaling pathways. RNA transcription and post-transcriptional regulation were the primary perturbed functions. Finally, 12 lincRNAs, six miRNAs and 47 mRNAs were included in a lincRNA-miRNA-mRNA network, and lincRNA0926-miR-190a-5p-Celf4 interactions may play a pivotal role in this regulatory network. Conclusion: This study provides clues for understanding the molecular basis of gut microbiota-brain interactions in depressive- and anxiety-like behaviors.