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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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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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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.
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Gut-brain actions underlying comorbid anxiety and depression associated with inflammatory bowel disease.
UNLABELLED: IntroductionInflammatory bowel disease (IBD) is a chronic relapsing and remitting disorder characterised by inflammation of the gastrointestinal tract. There is a growing consensus that IBD is associated with anxiety- and depression-related symptoms. Psychological symptoms appear to be more prevalent during active disease states with no difference in prevalence between Crohn's disease and ulcerative colitis. Behavioural disturbances including anxiety- and depression-like symptoms have also been observed in animal models of IBD. RESULTS: The likely mechanisms underlying the association are discussed with particular reference to communication between the gut and brain. The close bidirectional relationship known as the gut-brain axis includes neural, hormonal and immune communication links. Evidence is provided for a number of interacting factors including activation of the inflammatory response system in the brain, the hypothalamic-pituitary-adrenal axis, and brain areas implicated in altered behaviours, changes in blood brain barrier integrity, and an emerging role for gut microbiota and response to probiotics in IBD.DiscussionThe impact of psychological stress in models of IBD remains somewhat conflicted, however, it is weighted in favour of stress or early stressful life events as risk factors in the development of IBD, stress-induced exacerbation of inflammation and relapse. CONCLUSION: It is recommended that patients with IBD be screened for psychological disturbance and treated accordingly as intervention can improve quality of life and may reduce relapse rates.
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A biotin-free diet attenuates the incidence of collagen-induced arthritis and alleviates microbial dysbiosis.
Emerging evidence has shown that the gut microbiota and its products are important triggers in the pathogenesis of rheumatoid arthritis (RA). Biotin is a diet- and microbiome-dependent metabolite and an immune regulator; however, the role of biotin in RA remains unknown. In this study, we observed abnormal fecal biotin excretion in RA patients, which correlated with microbial alterations. Specifically, biotin content was inversely associated with gut microbial genera enriched in healthy controls, including Roseburia and Dorea. Meanwhile, it positively correlated with Oscillospira, which was highly enriched in RA individuals. Moreover, collagen-induced arthritis (CIA) mice fed a biotin-free diet had attenuated arthritis incidence with depressed differentiation of splenic CD3+ T cells and restored microbial diversities. The biotin-free diet also increased bone mass and protected against inflammation-induced bone loss in CIA mice. Additionally, the biotin-free diet reshaped the host metabolic phenotype of amino acids and microbial composition. Notably, biotin deficiency ameliorated the augmentation of Oscillospira in CIA mice. Collectively, our results suggested a potential link between biotin deficiency, gut microbiota dysbiosis and CIA progression.
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Microbiota-driven transcriptional changes in prefrontal cortex override genetic differences in social behavior.
Gene-environment interactions impact the development of neuropsychiatric disorders, but the relative contributions are unclear. Here, we identify gut microbiota as sufficient to induce depressive-like behaviors in genetically distinct mouse strains. Daily gavage of vehicle (dH2O) in nonobese diabetic (NOD) mice induced a social avoidance behavior that was not observed in C57BL/6 mice. This was not observed in NOD animals with depleted microbiota via oral administration of antibiotics. Transfer of intestinal microbiota, including members of the Clostridiales, Lachnospiraceae and Ruminococcaceae, from vehicle-gavaged NOD donors to microbiota-depleted C57BL/6 recipients was sufficient to induce social avoidance and change gene expression and myelination in the prefrontal cortex. Metabolomic analysis identified increased cresol levels in these mice, and exposure of cultured oligodendrocytes to this metabolite prevented myelin gene expression and differentiation. Our results thus demonstrate that the gut microbiota modifies the synthesis of key metabolites affecting gene expression in the prefrontal cortex, thereby modulating social behavior.
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Therapeutic potential of faecal microbiota transplantation for alcohol use disorder, a narrative synthesis.
BACKGROUND: Faecal microbiota transplantation is proposed as an alternative therapy to treat alcohol use disorder and has completed a Phase 1 clinical trial, with a Phase 2 clinical trial underway. Alcohol, a modifiable risk factor for noncommunicable diseases, resulted in approximately 3 million global deaths (5 %) in 2016 according to the World Health Organization. AIMS: A narrative synthesis examines the effects of alcohol and faecal microbiota transplantation on gut microbiota and how gut microbiota impacts the gut-brain axis, leading to certain behavioural symptoms of alcohol use disorder. These behavioural symptoms are alcohol craving and relapse in humans; and preference for alcohol, anxiety and depression in rodents. SEARCH METHODS AND RESULTS: Electronic databases PubMed, Embase, and Scopus were searched in January 2024 using the terms: faecal microbiota trans* AND alcohol AND microbio*. Ten studies out of 964 met the inclusion criteria of published primary studies with faecal microbiota transplantation as an intervention to study the gut-brain axis in alcohol use disorder. RESULTS: The gut microbiota is altered in alcohol use disorder, which can be modified with faecal microbiota transplantation. Behavioural symptoms such as alcohol craving and relapse are associated with inflammation due to a loss of intestinal barrier function. Beneficial microbiota produce short-chain fatty acids that maintain intestinal barrier function and reduce inflammation. Studies also reported anxiety and depression-like behaviours, in addition to a preference for alcohol in alcohol-naïve rodents after faecal microbiota transplantation from patients with alcohol use disorder. CONCLUSIONS: Faecal microbiota transplantation may moderate the behavioural symptoms of alcohol use disorder by altering gut microbiota, affecting intestinal permeability and inflammation, however, specific gut microbiota composition and long-term treatment outcomes require further clinical studies.
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Stress and mental health symptoms in early pregnancy are associated with the oral microbiome.
BACKGROUND: Research has revealed associations between microbes of the gastrointestinal tract and stress, anxiety and depression in pregnant or postpartum women. While these studies suggest a gut-brain-behaviour axis, no studies have examined microbes of the oral cavity in relation to maternal mental health. OBJECTIVE: To explore a potential oral-brain-behaviour axis related to maternal mental health. METHODS: Microbes were measured in saliva obtained from 224 second-trimester (mean±SD = 17±2 weeks) women oversampled for stress. Oralome data were associated with women's recent or cumulative pregnancy stress, trait and state anxiety, depression symptoms and post-traumatic stress disorder (PTSD) symptoms. Covariates explored included age, income, alcohol and tobacco use, dental issues and physical health problems. RESULTS: Pregnant women in the high trait anxiety or depression symptom groups had higher oral alpha diversity, indicating higher richness of species within samples. Groups with high and low PTSD symptoms differed in beta diversity, reflecting differences in community composition. Linear discriminant analysis showed differently abundant microbes in women with high stress versus low life stress, anxiety, depression, and PTSD, with the affected microbes mostly differing by symptom. Notably, members of phylum Proteobacteria were more abundant in women with high recent life stress and Spirochaetes was more abundant in women with high depression symptoms. Members of phylum Firmicutes were more abundant in the high trait anxiety and high depression groups. Genus Dialister (previously found to be lower in the gut of depressed non-pregnant people) was higher in women experiencing either high trait or state anxiety, or experiencing high depression symptoms, while genus Eikenella was elevated with high trait anxiety, depression or PTSD. CONCLUSIONS: The oral microbiome is associated with stress and mental health in pregnant women, in ways different from the gut microbiome or what has been found in non-pregnant people. CLINICAL IMPLICATIONS: Understanding oral microbiome-mental health relations may reveal future microbial targets to improve maternal psychological well-being.
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Circadian rhythms, gut microbiota, and diet: Possible implications for health.
AIMS: Over the past years, interest in chrono-nutrition has grown enormously as the fundamental role of circadian rhythms in regulating most physiological and metabolic processes has become clearer. Recently, the influence of circadian rhythms on the gut microbiota (GM) composition has also emerged, as more than half of the total microbial composition fluctuates rhythmically throughout the day. At the same time, other studies have observed that the GM itself synchronises the host's circadian biological clock through signals of a different nature. Therefore, it has been hypothesised that there is a two-way communication between the circadian rhythms of the host and the GM, but researchers have only just begun to identify some of its action mechanisms. The manuscript aim is, therefore, to gather and combine the latest evidence in the field of chrono-nutrition with the more recent research on the GM, in order to investigate their relationship and their potential impact on human health. DATA SYNTHESIS: Considering current evidence, a desynchronization of circadian rhythms is closely associated with an alteration in the abundance and functionality of the gut microbiota with consequent deleterious effects on health, such as increased risk of numerous pathologies, including cardiovascular disease, cancer, irritable bowel disease, and depression. A key role in maintaining the balance between circadian rhythms and GM seems to be attributed to meal-timing and diet quality, as well as to certain microbial metabolites, in particular short-chain fatty acids. CONCLUSIONS: Future studies are needed to decipher the link between the circadian rhythms and specific microbial patterns in relation to different disease frameworks.
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Extracellular Vesicles from Gram-positive and Gram-negative Probiotics Remediate Stress-Induced Depressive Behavior in Mice.
Chronic stress causes maladaptive changes in the brain that lead to depressive behavior. In the present study, we investigate whether chronic stress alters gut microbiota compositions that are related to stress-induced maladaptive changes in the brain. Mice treated with daily 2-h restraint for 14 days (CRST) exhibit depressive-like behavior. Sequence readings of 16S rRNA genes prepared from fecal samples taken from CRST-treated mice suggest that chronic stress induces gut microbiota changes that are pronounced in the post-stress period, relative to those that occur in the 14-day stress phase. The genus Lactobacillus is one such microbiota substantially changed following chronic stress. In contrast, intraperitoneal injection of extracellular vesicles (EVs) isolated from culture media of the Gram-positive probiotic Lactobacillus plantarum is sufficient to ameliorate stress-induced depressive-like behavior. Interestingly, EVs from the Gram-positive probiotic Bacillus subtilis and EVs from the Gram-negative probiotic Akkermansia muciniphila also produce anti-depressive-like effects. While chronic stress decreases the expression of MeCP2, Sirt1, and/or neurotrophic factors in the hippocampus, EVs from the three selected probiotics differentially restore stress-induced changes of these factors. These results suggest that chronic stress produces persistent changes in gut microbiota composition, whereas purified EVs of certain probiotics can be used for treatment of stress-induced depressive-like behavior.