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Prenatal stress affects placental cytokines and neurotrophins, commensal microbes, and anxiety-like behavior in adult female offspring.
Recent studies demonstrate that exposure to stress changes the composition of the intestinal microbiota, which is associated with development of stress-induced changes to social behavior, anxiety, and depression. Stress during pregnancy has also been related to the emergence of these disorders; whether commensal microbes are part of a maternal intrauterine environment during prenatal stress is not known. Here, we demonstrate that microbiome changes are manifested in the mother, and also found in female offspring in adulthood, with a correlation between stressed mothers and female offspring. Alterations in the microbiome have been shown to alter immune responses, thus we examined cytokines in utero. IL-1β was increased in placenta and fetal brain from offspring exposed to the prenatal stressor. Because IL-1β has been shown to prevent induction of brain derived neurotrophic factor (BDNF), we examined BDNF and found a reduction in female placenta and adult amygdala, suggesting in utero impact on neurodevelopment extending into adulthood. Furthermore, gastrointestinal microbial communities were different in adult females born from stressed vs. non-stressed pregnancies. Adult female offspring also demonstrated increased anxiety-like behavior and alterations in cognition, suggesting a critical window where stress is able to influence the microbiome and the intrauterine environment in a deleterious manner with lasting behavioral consequences. The microbiome may be a key link between the intrauterine environment and adult behavioral changes.
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Intestinal mycobiota dysbiosis associated inflammation activation in chronic schizophrenia.
The microbiome-gut-brain axis is related to schizophrenia (SCZ). The role of intestinal mycobiota in SCZ has been under investigated. We present a half-year follow-up study involving 109 chronic SCZ patients and 77 healthy controls. Intestinal mycobiota was tested by internal transcribed spacer (ITS). Untargeted liquid chromatography-mass spectrometry (LC-MS) was used to measure fecal metabolites. Symptom severity was assessed using the Positive and Negative Syndrome Scale. Enterotype analysis showed that Candida-type patients exhibited severer positive symptoms and depression factors than Saccharomyces-type patients. Candida and its top species and operational taxonomic units (OTUs) were positively correlated with depression factors (all p=0.001). Fecal metabolites analysis showed that upregulated metabolites were associated with chronic inflammation (NF-κB pathway and T helper cell differentiation), downregulated metabolites were associated with glutamate metabolism, serotonergic and dopaminergic synapse. Procrustes analysis revealed significant correlation between intestinal mycobiota and fecal metabolites (M2=0.937, p<0.001). Metabolic module analysis showed that the top module, MEturquoise (associated with Th1 and Th2 cell differentiation), was negatively correlated with SCZ (r=-0.783, p<0.0001), positively correlated with Candida, Aspergillus, Trichosporon and Talaromyces (decreased in SCZ) and negatively correlated with Saccharomyces (increased in SCZ). We also found impairments of intestinal barrier in SCZ, characterized by increased in blood D-lactate (mucosa impairment marker) and decreased in blood mucin 2 (mucosal barrier protective protein). Serum levels of TNF-α was increased and showed stable high levels during treatment. This study suggests that mycobiota dysbiosis-related chronic inflammation and an impaired intestinal mucosal barrier are associated with chronic SCZ.
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A Multicenter Randomized Controlled Trial of Microbiome-Based Artificial Intelligence-Assisted Personalized Diet vs Low-Fermentable Oligosaccharides, Disaccharides, Monosaccharides, and Polyols Diet: A Novel Approach for the Management of Irritable Bowel Syndrome.
INTRODUCTION: Personalized management strategies are pivotal in addressing irritable bowel syndrome (IBS). This multicenter randomized controlled trial focuses on comparing the efficacy of a microbiome-based artificial intelligence-assisted personalized diet (PD) with a low-fermentable oligosaccharides, disaccharides, monosaccharides, and polyols diet (FODMAP) for IBS management. METHODS: One hundred twenty-one patients participated, with 70 assigned to the PD group and 51 to the FODMAP diet group. IBS subtypes, demographics, symptom severity (IBS-SSS), anxiety, depression, and quality of life (IBS-QOL) were evaluated. Both interventions spanned 6 weeks. The trial's primary outcome was the within-individual difference in IBS-SSS compared between intervention groups. RESULTS: For the primary outcome, there was a change in IBS-SSS of -112.7 for those in the PD group vs -99.9 for those in the FODMAP diet group ( P = 0.29). Significant improvement occurred in IBS-SSS scores ( P < 0.001), frequency ( P < 0.001), abdominal distension ( P < 0.001), and life interference ( P < 0.001) in both groups. In addition, there were significant improvements in anxiety levels and IBS-QOL scores for both groups ( P < 0.001). Importantly, PD was effective in reducing IBS SSS scores across all IBS subtypes IBS-Constipation (IBS-C; P < 0.001), IBS-Diarrhea (IBS-D; P = 0.01), and IBS-Mixed (IBS-M; P < 0.001) while FODMAP diet exhibited comparable improvements in IBS-C ( P = 0.004) and IBS-M ( P < 0.001). PD intervention significantly improved IBS-QOL scores for all subtypes (IBS-C [ P < 0.001], IBS-D [ P < 0.001], and IBS-M [ P = 0.008]) while the FODMAP diet did so for the IBS-C ( P = 0.004) and IBS-D ( P = 0.022). Notably, PD intervention led to significant microbiome diversity shifts ( P < 0.05) and taxa alterations compared with FODMAP diet. DISCUSSION: The artificial intelligence-assisted PD emerges as a promising approach for comprehensive IBS management. With its ability to address individual variation, the PD approach demonstrates significant symptom relief, enhanced QOL, and notable diversity shifts in the gut microbiome, making it a valuable strategy in the evolving landscape of IBS care.
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Inulin ameliorates schizophrenia via modulation of the gut microbiota and anti-inflammation in mice.
The microbiome-gut-brain (MGB) axis, which regulates neurological and cognitive functions, plays an essential role in schizophrenia (SCZ) progression. Dietary inulin could be a novel strategy for the treatment of SCZ due to its modulating effects on the gut microbiota. In this study, the effects of inulin on mice with SCZ were studied. As indicated by the behavioural tests, expression of neurotransmitters, inflammatory indicators, and brain morphology, inulin administration ameliorated aberrant behaviours (locomotor hypoactivity, anxiety disorders and depressive behaviours, and impaired learning and spatial recognition memory) and effectively reduced neuroinflammation and neuronal damage. In addition, inulin improved intestinal integrity and permeability, as indicated by the elevated expression of tight junction proteins (p < 0.05). The results of 16S rRNA sequencing and analysis showed that inulin increased the abundance of Lactobacillus and Bifidobacterium, which were negatively correlated with 5-hydroxytryptamine and inflammatory cytokines and positively correlated with brain-derived neurotrophic factor (BDNF). Inulin caused a reduction in Akkermansia that was positively correlated with inflammatory cytokines and negatively correlated with BDNF. These results suggested that dietary inulin modulated the gut microbiota and exerted anti-inflammatory effects in mice though the MGB axis, which further ameliorated SCZ. Therefore, the results of this study provide a potential explanation for inulin intervention in the treatment of SCZ.
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Gut-brain Axis: Role of Lipids in the Regulation of Inflammation, Pain and CNS Diseases.
The human gut is a composite anaerobic environment with a large, diverse and dynamic enteric microbiota, represented by more than 100 trillion microorganisms, including at least 1000 distinct species. The discovery that a different microbial composition can influence behavior and cognition, and in turn the nervous system can indirectly influence enteric microbiota composition, has significantly contributed to establish the well-accepted concept of gut-brain axis. This hypothesis is supported by several evidence showing mutual mechanisms, which involve the vague nerve, the immune system, the hypothalamic-pituitaryadrenal (HPA) axis modulation and the bacteria-derived metabolites. Many studies have focused on delineating a role for this axis in health and disease, ranging from stress-related disorders such as depression, anxiety and irritable bowel syndrome (IBS) to neurodevelopmental disorders, such as autism, and to neurodegenerative diseases, such as Parkinson Disease, Alzheimer's Disease etc. Based on this background, and considering the relevance of alteration of the symbiotic state between host and microbiota, this review focuses on the role and the involvement of bioactive lipids, such as the N-acylethanolamine (NAE) family whose main members are N-arachidonoylethanolamine (AEA), palmitoylethanolamide (PEA) and oleoilethanolamide (OEA), and short chain fatty acids (SCFAs), such as butyrate, belonging to a large group of bioactive lipids able to modulate peripheral and central pathologic processes. Their effective role has been studied in inflammation, acute and chronic pain, obesity and central nervous system diseases. A possible correlation has been shown between these lipids and gut microbiota through different mechanisms. Indeed, systemic administration of specific bacteria can reduce abdominal pain through the involvement of cannabinoid receptor 1 in the rat; on the other hand, PEA reduces inflammation markers in a murine model of inflammatory bowel disease (IBD), and butyrate, producted by gut microbiota, is effective in reducing inflammation and pain in irritable bowel syndrome and IBD animal models. In this review, we underline the relationship among inflammation, pain, microbiota and the different lipids, focusing on a possible involvement of NAEs and SCFAs in the gut-brain axis and their role in the central nervous system diseases.
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Role of the gut microbiota in complications after ischemic stroke.
Ischemic stroke (IS) is a serious central nervous system disease. Post-IS complications, such as post-stroke cognitive impairment (PSCI), post-stroke depression (PSD), hemorrhagic transformation (HT), gastrointestinal dysfunction, cardiovascular events, and post-stroke infection (PSI), result in neurological deficits. The microbiota-gut-brain axis (MGBA) facilitates bidirectional signal transduction and communication between the intestines and the brain. Recent studies have reported alterations in gut microbiota diversity post-IS, suggesting the involvement of gut microbiota in post-IS complications through various mechanisms such as bacterial translocation, immune regulation, and production of gut bacterial metabolites, thereby affecting disease prognosis. In this review, to provide insights into the prevention and treatment of post-IS complications and improvement of the long-term prognosis of IS, we summarize the interaction between the gut microbiota and IS, along with the effects of the gut microbiota on post-IS complications.
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Fermented foods and brain health: Gut-brain axis mechanisms and clinical insights.
The gut-brain axis represents a complex bidirectional communication network connecting the central nervous and gastrointestinal systems. Fermented foods and their phenolic compounds, which increase their bioavailability due to microbial transformation in their contents, have the potential to affect the gut microbiota and therefore the gut-brain axis positively. Fermented foods such as kefir, yogurt, miso, natto, tempeh, kombucha, and their polyphenols have an effect on the gut microbiota and on the provision of neurological activities through neuroactive components that affect the nervous system. Phenolic compounds appear to have direct or indirect effects on brain tissue through various mechanisms such as reducing neuronal oxidative stress, suppressing microglial activation, supporting synaptic plasticity, and slowing down neurodegenerative processes such as Alzheimer's and Parkinson's. In addition, the polyphenol content enriched in fermented foods has been shown to exhibit psychobiotic effects in depression and anxiety models; it has been shown in clinical studies that it improves systemic inflammation and hypothalamic-pituitary-adrenal (HPA) axis dysfunction. Current data support the inclusion of fermented, polyphenol-rich foods as a noninvasive strategy to enhance neuroprotection and mental health. However, enhanced clinical studies are needed where heterogeneity in the fermentation process and dosage adjustment are standardized. This article reviews the current literature on the effects of fermented foods and polyphenols on brain health via the microbiota and gut-brain axis.
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The interaction between tea polyphenols and host intestinal microorganisms: an effective way to prevent psychiatric disorders.
Tea polyphenols (TP) are the most bioactive components in tea extracts. It has been reported that TP can regulate the composition and the function of the intestinal flora. Meanwhile, intestinal microorganisms improve the bioavailability of TP, and the corresponding metabolites of TP can regulate intestinal micro-ecology and promote human health more effectively. The dysfunction of the microbiota-gut-brain axis is the main pathological basis of depression, and its abnormality may be the direct cause and potential influencing factor of psychiatric disorders. The interrelationship between TP and intestinal microorganisms is discussed in this review, which will enable us to better evaluate the potential preventive effects of TP on psychiatric disorders by modulating host intestinal microorganisms.
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Tryptophan Metabolism: A Link Between the Gut Microbiota and Brain.
The gut-brain axis (GBA) is a bilateral communication network between the gastrointestinal (GI) tract and the central nervous system. The essential amino acid tryptophan contributes to the normal growth and health of both animals and humans and, importantly, exerts modulatory functions at multiple levels of the GBA. Tryptophan is the sole precursor of serotonin, which is a key monoamine neurotransmitter participating in the modulation of central neurotransmission and enteric physiological function. In addition, tryptophan can be metabolized into kynurenine, tryptamine, and indole, thereby modulating neuroendocrine and intestinal immune responses. The gut microbial influence on tryptophan metabolism emerges as an important driving force in modulating tryptophan metabolism. Here, we focus on the potential role of tryptophan metabolism in the modulation of brain function by the gut microbiota. We start by outlining existing knowledge on tryptophan metabolism, including serotonin synthesis and degradation pathways of the host, and summarize recent advances in demonstrating the influence of the gut microbiota on tryptophan metabolism. The latest evidence revealing those mechanisms by which the gut microbiota modulates tryptophan metabolism, with subsequent effects on brain function, is reviewed. Finally, the potential modulation of intestinal tryptophan metabolism as a therapeutic option for brain and GI functional disorders is also discussed.
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Sex hormones and functional gastrointestinal disorders in menopausal women.
Functional gastrointestinal diseases (FGIDs)/disorders of gut-brain interaction (DGBI) that manifest during menopause are characterized by chronic recurrent gastrointestinal (GI) symptoms associated with fluctuations in sex hormones. Current research indicates that the regulatory influence of sex hormones on GI function is multifaceted, involving a complex endocrine regulatory network across multiple organs and systems. Various types of sex hormones exert both direct and indirect effects on GI function through their specific receptors located within the GI tract, the central nervous system, pancreatic islets, and thyroid tissue. This interplay contributes to the pathological and physiological mechanisms underlying the onset of menopausal FGIDs/DGBI. Simultaneously, these interactions create a complex pathological feedback loop with climacteric syndrome, depression/anxiety, and sleep disorders. In this study, we present a comprehensive narrative review detailing the molecular mechanisms by which sex hormones regulate GI function-both directly and indirectly-as well as examining the impact of clinical hormone replacement therapy on GI functionality. Our objective is to elucidate potential pathogenesis pathways for FGIDs/DGBI in menopausal women linked to changes in sex hormone levels, further clarify the relationship between hormonal fluctuations and GI function, and propose new therapeutic strategies for managing FGIDs/DGBI. Additionally, alterations in gut microbiota may play a significant role in mediating interactions between sex hormones and the gut-brain axis. This exploration also offers fresh insights and avenues for future clinical research into the relationship between sex hormones and FGIDs/DGBI.