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Akkermansia muciniphila in neuropsychiatric disorders: friend or foe?
An accumulating body of evidence suggests that the bacterium Akkermansia muciniphila exhibits positive systemic effects on host health, mainly by improving immunological and metabolic functions, and it is therefore regarded as a promising potential probiotic. Recent clinical and preclinical studies have shown that A. muciniphila plays a vital role in a variety of neuropsychiatric disorders by influencing the host brain through the microbiota-gut-brain axis (MGBA). Numerous studies observed that A. muciniphila and its metabolic substances can effectively improve the symptoms of neuropsychiatric disorders by restoring the gut microbiota, reestablishing the integrity of the gut mucosal barrier, regulating host immunity, and modulating gut and neuroinflammation. However, A. muciniphila was also reported to participate in the development of neuropsychiatric disorders by aggravating inflammation and influencing mucus production. Therefore, the exact mechanism of action of A. muciniphila remains much controversial. This review summarizes the proposed roles and mechanisms of A. muciniphila in various neurological and psychiatric disorders such as depression, anxiety, Parkinson's disease, Alzheimer's disease, multiple sclerosis, strokes, and autism spectrum disorders, and provides insights into the potential therapeutic application of A. muciniphila for the treatment of these conditions.
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Impact of outdoor nature-related activities on gut microbiota, fecal serotonin, and perceived stress in preschool children: the Play&Grow randomized controlled trial.
Due to rapid urbanization, children today have fewer opportunities to interact with nature and this may result in a greater risk for developing stress and depression. Outdoor nature-related activities can enhance general well-being. However, the underlying mechanisms are not fully delineated. Here we recruited 54 preschool children to participate in a 10-week structured nature-related "Play&Grow" program. Following the intervention, children were assessed for connectedness to nature and perceived stress levels using validated questionnaires. Moreover, fecal serotonin level and gut microbiota profiles were measured by ELISA and 16S rDNA amplicon sequencing, respectively. Children were significantly more connected to nature after the intervention. Their gut microbiota altered, especially by modulating the abundance of Roseburia and the fecal-serotonin level. Moreover, we also observed a reduction in the overall perceived stress, particularly in the frequency of anger among these children. This study is the first to demonstrate the impact of nature-related activities on gut microbiota, fecal serotonin and psychosocial behaviour of preschool children. However, further mechanistic studies are needed to confirm the functional role of gut microbiota in the association between connectedness to nature and improved psychosocial behavior.
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Defining Dysbiosis in Disorders of Movement and Motivation.
The gut microbiota has emerged as a critical player in shaping and modulating brain function and has been shown to influence numerous behaviors, including anxiety and depression-like behaviors, sociability, and cognition. However, the effects of the gut microbiota on specific disorders associated with thalamo-cortico-basal ganglia circuits, ranging from compulsive behavior and addiction to altered sensation and motor output, are only recently being explored. Wholesale depletion and alteration of gut microbial communities in rodent models of disorders, such as Parkinson's disease, autism, and addiction, robustly affect movement and motivated behavior. A new frontier therefore lies in identifying specific microbial alterations that affect these behaviors and understanding the underlying mechanisms of action. Comparing alterations in gut microbiota across multiple basal-ganglia associated disease states allows for identification of common mechanistic pathways that may interact with distinct environmental and genetic risk factors to produce disease-specific outcomes.
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The Role of the Aryl Hydrocarbon Receptor (AHR) in Immune and Inflammatory Diseases.
The aryl hydrocarbon receptor (AHR) is a nuclear receptor that modulates the response to environmental stimuli. It was recognized historically for its role in toxicology but, in recent decades, it has been increasingly recognized as an important modulator of disease-especially for its role in modulating immune and inflammatory responses. AHR has been implicated in many diseases that are driven by immune/inflammatory processes, including major depressive disorder, multiple sclerosis, rheumatoid arthritis, asthma, and allergic responses, among others. The mechanisms by which AHR has been suggested to impact immune/inflammatory diseases include targeted gene expression and altered immune differentiation. It has been suggested that single nucleotide polymorphisms (SNPs) that are near AHR-regulated genes may contribute to AHR-dependent disease mechanisms/pathways. Further, we have found that SNPs that are outside of nuclear receptor binding sites (i.e., outside of AHR response elements (AHREs)) may contribute to AHR-dependent gene regulation in a SNP- and ligand-dependent manner. This review will discuss the evidence and mechanisms of AHR contributions to immune/inflammatory diseases and will consider the possibility that SNPs that are outside of AHR binding sites might contribute to AHR ligand-dependent inter-individual variation in disease pathophysiology and response to pharmacotherapeutics.
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Biodegradation of expanded polystyrene and low-density polyethylene foams in larvae of Tenebrio molitor Linnaeus (Coleoptera: Tenebrionidae): Broad versus limited extent depolymerization and microbe-dependence versus independence.
Yellow mealworms (Tenebrio molitor larvae) are capable of biodegrading polystyrene (PS) and low-density polyethylene (LDPE). This study tested biodegradation of one expanded PS (EPS) with a weight-average molecular weight (Mw) 256.4 kDa and two LDPE foams with respective Mw of 130.6 kDa (PE-1) and 288.7 kDa (PE-2) in T. monitor larvae obtained in Beijing, China. The larvae consumed EPS and both LDPEs over a 60 day. Fourier transform infrared spectroscopy and thermogravimetric analyses of frass confirmed the formation of new oxygen-containing functional groups, as well as a change in physical property and chemical modification, indicating that biodegradation of EPS and LDPE occurred. Gel permeation chromatography analysis confirmed broad depolymerization of EPS and PE-1 (i.e., a decrease in both Mw and a number-average molecular weight (Mn)) but revealed limited extent depolymerization of PE-2 (i.e., increase in Mn and decrease in Mw). For all materials, the size-average molecular weight (Mz) was decreased. Biodegradation and oxidation of EPS and LDPE were confirmed using FTIR and TGA analysis. Depression of gut microbes by the antibiotic gentamicin resulted in significant inhibition of EPS depolymerization but did not stop LDPE depolymerization, resulting in the increase in Mn and revealing that PS biodegradation was gut microbe-dependent but LDPE biodegradation was less dependent or independent of gut microbes. Gut microbial community analysis indicated that, as expected, under different dietary conditions, the intestinal flora significantly shifted to communities associated with biodegradation of EPS and LDPE. The results indicated the complexity and limitation of biodegradation of plastics in plastics-eating T. molitor larvae.
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Review of mechanisms of deoxynivalenol-induced anorexia: The role of gut microbiota.
Deoxynivalenol (DON) is one of the most important mycotoxins in cereal-based foods or other food productions, produced by Fusarium species. Because of the high occurrence of DON in food combined with vast consumption of cereals and grain worldwide, the DON-contaminated food is a very harmful factor for human and animal health. DON has been reported to induce anorexia at lower or chronic doses in animal models. However, further researches for DON-induced anorexia are limited. Previous publications demonstrated a close link between Bacteroidetes and Firmicutes, two kinds of gut microbiota, with weight loss and the effect of low administration of DON on neurotransmitters in the frontal cortex, cerebellum, hypothalamus, hippocampus and pons/medulla. These data are similar to other studies, which show selective 5HTα receptor agonists apparently causing hyperphagia whereas 5HT1β agonists appear to induce anorexia. Thus, the neurochemical effects of lower DON exposure can be as a result of peripheral toxicological events such as emesis, which overwhelmed its more subtle feed refusal activity. Besides, changes in the microbiota have an impact on stress-related behaviors like anxiety and depression, which can lead to weight loss through decreased feed intake. Gut dysbiosis is also associated with brain dysfunction and with behavioral changes. These conclusions illustrate as well a potential explanation for DON-induced anorexia.In this review, we summarize information about DON-induced anorexia from previous studies and provide our opinion for future investigations that could establish a link between gut microbiota, neurotransmitters, anorexia and weight loss under the DON exposure. Copyright © 2017 John Wiley & Sons, Ltd.
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Impact of long-term medication on estrobolome-associated β-glucuronidase and sulfatase activities: Implications for estrogen homeostasis in postmenopausal women.
Menopause leads to a decline in circulating estrogen levels, increasing cardiometabolic risk, contributing to bone loss, and decreasing quality of life. The estrobolome, a subset of microbes with β-glucuronidase (GUS) and sulfatase activities, regulates estrogen homeostasis through deconjugation and enterohepatic recycling, thereby influencing systemic estrogen availability. Common long-term pharmacological treatments in postmenopausal women may alter gut microbial composition and function, potentially affecting estrobolome activity and systemic estrogen levels. This narrative review examines current evidence on how long-term pharmacological treatments may affect estrobolome-associated GUS and sulfatase activities, with implications for estrogen metabolism and health outcomes in postmenopausal women. A targeted literature search was performed to identify clinical studies on commonly prescribed drugs for hypertension, diabetes, dyslipidemia, osteoporosis, and depression in postmenopausal women, focusing on microbial taxa with reported GUS or sulfatase activity. Among the evaluated pharmacological classes, antidiabetic drugs, particularly metformin, are the most extensively studied, followed by antidepressants. These treatments can modulate key gut bacterial genera with GUS and sulfatase activities, including Bifidobacterium, Roseburia, Faecalibacterium, and Clostridium, which are relevant to metabolic and estrogen homeostasis. However, no studies have directly assessed the impact of pharmacological treatments on GUS and sulfatase activity in postmenopausal women. Understanding how chronic medication influences estrobolome dynamics may help identify strategies to support estrogen balance and improve systemic metabolic, hormonal, vascular, and inflammatory profiles. This review highlights the interplay between long-term medication, gut microbiota, and estrogen homeostasis as a promising avenue for personalized microbiota-targeted therapies in postmenopausal health.
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The Microbiota, the Gut and the Brain in Eating and Alcohol Use Disorders: A 'Ménage à Trois'?
AIMS: Accumulating evidence for the influence of the gut microbiota on the bidirectional communication along the gut-brain axis suggests a role of the gut microbiota in eating disorders (EDs) and alcohol and substance use disorders. The potential influence of altered gut microbiota (dysbiosis) on behaviors associated with such disorders may have implications for developing therapeutic interventions. METHODS: A systematic review of preclinical and clinical studies evaluating the gut microbiota, EDs and alcohol and substance use disorders was conducted using MEDLINE, Embase and Web of Science databases with the objective being to examine the role of the gut microbiota in behavioral correlates of these disorders. Original papers focused on the gut microbiota and potential behavioral implications were deemed eligible for consideration. RESULTS: The resulting 12 publications were limited to gut microbiota studies related to EDs and alcohol and substance use disorders. Some studies suggest that dysbiosis and gut microbial byproducts may influence the pathophysiology of EDs via direct and indirect interference with peptide hormone signaling. Additionally, dysbiosis was shown to be correlated with alcohol use disorder-related symptoms, i.e. craving, depression and anxiety. Finally, a mouse study suggests that manipulations in the gut microbiota may affect cocaine-related behaviors. CONCLUSIONS: Promising, albeit preliminary, findings suggest a potential role of the gut microbiota in behavioral correlates of EDs and alcohol and substance use disorders. SHORT SUMMARY: Preliminary evidence exists supporting the role of the gut microbiota in eating disorders and alcohol and substance use disorders, although additional investigation is needed to determine what is causative versus epiphenomenological.
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Chronic Social Stress and Immune Dysregulation: Integrating Neuroendocrine Signaling, Microbiota, and Tissue-Specific Responses.
Psychological stress arises when individuals perceive demands as exceeding their capacity to cope. Social stress can be acute, such as giving a presentation, producing transient increases in heart rate, blood pressure, and neuroendocrine activation, or chronic, in which stressors persist over extended periods. Chronic psychosocial stress disrupts immune homeostasis and contributes to anxiety, depression, and post-traumatic stress, while also increasing risk for infections, inflammatory and autoimmune diseases, cardiovascular disease, metabolic dysfunction, and cancer. Persistent stress engages interconnected neuroendocrine-immune networks, including the hypothalamic-pituitary-adrenal axis, the sympathetic-adrenomedullary system, and the gut microbiota-brain-immune axis, leading to sustained glucocorticoid and catecholamine signaling, gut dysbiosis, impaired barrier integrity, and altered microbial metabolite profiles. In this review, we summarize the molecular and cellular mechanisms by which these axes remodel innate and adaptive immunity and shape disease susceptibility. Using social defeat and social isolation in mice as model systems, we highlight how chronic social stress reprograms immune responses in key tissues, including the lung, brain, and gut.
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The role of microbiota-gut-brain axis in neuropsychiatric and neurological disorders.
Emerging evidence indicates that the gut microbiota play a crucial role in the bidirectional communication between the gut and the brain suggesting that the gut microbes may shape neural development, modulate neurotransmission and affect behavior, and thereby contribute to the pathogenesis and/or progression of many neurodevelopmental, neuropsychiatric, and neurological conditions. This review summarizes recent data on the role of microbiota-gut-brain axis in the pathophysiology of neuropsychiatric and neurological disorders including depression, anxiety, schizophrenia, autism spectrum disorders, Parkinson's disease, migraine, and epilepsy. Also, the involvement of microbiota in gut disorders co-existing with neuropsychiatric conditions is highlighted. We discuss data from both in vivo preclinical experiments and clinical reports including: (1) studies in germ-free animals, (2) studies exploring the gut microbiota composition in animal models of diseases or in humans, (3) studies evaluating the effects of probiotic, prebiotic or antibiotic treatment as well as (4) the effects of fecal microbiota transplantation.