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Novel aspects of enteric serotonergic signaling in health and brain-gut disease.
Gastrointestinal (GI) comorbidities are common in individuals with mood and behavioral dysfunction. Similarly, patients with GI problems more commonly suffer from co-morbid psychiatric diagnoses. Although the central and enteric nervous systems (CNS and ENS, respectively) have largely been studied separately, there is emerging interest in factors that may contribute to disease states involving both systems. There is strong evidence to suggest that serotonin may be an important contributor to these brain-gut conditions. Serotonin has long been recognized for its critical functions in CNS development and function. The majority of the body's serotonin, however, is produced in the GI tract, where it plays key roles in ENS development and function. Further understanding of the specific impact that enteric serotonin has on brain-gut disease may lay the foundation for the creation of novel therapeutic targets. This review summarizes the current data focusing on the important roles that serotonin plays in ENS development and motility, with a focus on novel aspects of serotonergic signaling in medical conditions in which CNS and ENS co-morbidities are common, including autism spectrum disorders and depression.
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Microbiota alterations are related to migraine food triggers and inflammatory markers in chronic migraine patients with medication overuse headache.
OBJECTIVE: Chronic migraine (CM) patients with medication overuse headache (MOH) were recently shown to be associated with leaky gut and inflammation. We aimed to investigate gut microbiota profiles of CM patients with MOH, and their correlations with inflammatory serum parameters, migraine food triggers, and comorbid anxiety and depression. MATERIALS AND METHODS: The study included women participants (32 CM patients with NSAID overuse headache, and 16 healthy non-headache sufferers). Migraine duration, monthly migraine headache days, presence of irritable bowel syndrome symptoms, and HADS-D and HADS-A scores were recorded. Serum samples were collected to measure circulating LPS, HMGB1, HIF-1α, and IL-6. The gut microbiota profiles of the patients were evaluated using fecal samples. RESULTS: Serum LPS, HMGB1, HIF-1α, and IL-6 levels were significantly higher in the CM + MOH group compared to the healthy controls. HADS-A and HADS-D scores were considerably higher in the CM + MOH group compared to the healthy controls. In the microbiota analysis, alpha and beta diversities were similar between the two groups. The class Clostridia, the order Eubacteriales, and the genus Ruminococcus were less abundant in the CM + NSAID overuse headache group compared to the control group. At the genus level Desulfovibrio, Gemmiger, and Dialister and at the species level, Clostridium fessum, Blautia luti, Dorea longicatena, Eubacterium coprostanoligenes, and Gemmiger formicilis were more abundant in the CM + NSAID overuse headache group compared to the control group. Desulfovibrio, Gemmiger, Dialister, Ethanoligenens harbinense, Eubacterium coprostanoligenes, Dorea longicatena, and Thermoclostridium stercorarium showed positive correlations and Clostridia bacteria showed negative correlations with migraine food triggers. Positive correlations were found between LPS and Hapalosiphonaceae, HMGB1 and Melghirimyces, HIF1-α and Rouxeilla and Blautia luti, IL-6 and Melghirimyces and Ruminococcus. CONCLUSION: In CM patients with MOH, we have revealed the presence of dysbiosis towards an inflammatory state, and positive correlations were shown between altered gut microbiota and inflammatory serum parameters and migraine food triggers.
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Advances in the study of the relationship between gut microbiota and erectile dysfunction.
INTRODUCTION: In recent years, in-depth research has revealed that gut microbiota has an inseparable relationship with erectile dysfunction (ED) in men. OBJECTIVES: (1) To review the correlation between gut microbiota and ED from the perspective of its impact on men's mental health, metabolism, immunity, and endocrine regulation and (2) to provide reference to further explore the pathogenesis of ED and the improvement of clinical treatment plans. METHODS: PubMed was used for the literature search to identify publications related to ED and gut microbiota. RESULTS: Gut microbiota may induce depression and anxiety through the microbiota-gut-brain axis, leading to the occurrence of psychological ED. It may also cause vascular endothelial dysfunction and androgen metabolism disorder by interfering with lipid metabolism, immunity, and endocrine regulation, leading to the occurrence of organic ED. CONCLUSION: Gut microbiota and its metabolites play an important role in the occurrence and development of ED. As a new influencing factor of ED, gut microbiota disorder is expected to become a target for treatment.
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Current evidence linking diet to gut microbiota and brain development and function.
The gut:brain axis is emerging as an important information highway linking the foods we eat with neurophysiological development and functions. Some gut microorganisms have shown to alleviate anxiety and depression, improve cognitive performance and play a role in brain development in early life. However, most studies were conducted in laboratory animals and these findings await confirmation in carefully designed human interventions. Similarly, little attention has been given to how diet:microbe interactions within the gut can impact on neurotransmitter production or their subsequent biological effects within the nervous system. In this review, we discuss the possible influence of carbohydrates, polyphenols, lipids and proteins colonic fermentation on production, bioavailability and biological activity of metabolites linked to the gut-microbiota-brain axis. An increased understanding of how nervous system may be regulated by diet will greatly enhance our ability to design dietary strategies to improve healthy brain development and functions.
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Microbiota-gut-brain signalling in Parkinson's disease: Implications for non-motor symptoms.
Parkinson's disease is the second most common neurodegenerative disorder, affecting 1-2% of the population over 65 years of age. The primary neuropathology is the loss of midbrain dopaminergic neurons, resulting in characteristic motor deficits, upon which the clinical diagnosis is based. However, a number of significant non-motor symptoms (NMS) are also evident that appear to have a greater impact on the quality of life of these patients. In recent years, it has become increasingly apparent that neurobiological processes can be modified by the bi-directional communication that occurs along the brain-gut axis. The microbiota plays a key role in this communication throughout different routes in both physiological and pathological conditions. Thus, there has been an increasing interest in investigating how microbiota changes within the gastrointestinal tract may be implicated in health and disease including PD. Interestingly α-synuclein-aggregates, the cardinal neuropathological feature in PD, are present in both the submucosal and myenteric plexuses of the enteric nervous system, prior to their appearance in the brain, indicating a possible gut to brain route of "prion-like" spread. In this review we highlight the potential importance of gut to brain signalling in PD with particular focus on the role of the microbiota as major player in this communication.
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The correlation between intestinal dysbiosis and the development of ankylosing spondylitis.
The pathogenesis and development of ankylosing spondylitis (AS) is concealed and complicated. In recent years, alterations in gut microbiota of AS patients have been largely investigated, although the underlying mechanisms remain unclear. This article reviews the recent studies on changes of gut microbiota in AS patients, and discusses the possible correlation between intestinal dysbiosis and AS development from aspects including genetic factor HLA-B27, mucosal immune responses and the depression accompanying AS.
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Diabesity and mood disorders: Multiple links through the microbiota-gut-brain axis.
The global prevalence of diabesity is on the rise, and the clinical, social and economic health burden arising from this epidemic is aggravated by a significant co-morbidity of diabesity with neuropsychiatric disease, particularly depression. Importantly, not only is the prevalence of mood disorders elevated in patients with type 2 diabetes, depressed patients are also more prone to develop diabetes. This reciprocal relationship calls for a molecular and systemic analysis of diabesity-brain interactions to guide preventive and therapeutic strategies. The analysis we are presenting in this review is modelled on the microbiota-gut-brain axis, which provides the brain with information from the gut not only via the nervous system, but also via a continuous stream of microbial, endocrine, metabolic and immune messages. This communication network offers important clues as to how obesity and diabetes could target the brain to provoke neuropsychiatric disease. There is emerging evidence that the gut microbiota is orchestrating a multiplicity of bodily functions that are intimately related to the immune, metabolic and nervous systems and that gut dysbiosis spoils the homeostasis between these systems. In our article we highlight two groups of molecular links that seem to have a significant bearing on the impact of diabesity on the brain. On the one hand, we focus on microbiota-related metabolites such as short-chain fatty acids, tryptophan metabolites, immune stimulants and endocannabinoids that are likely to play a mediator role. On the other hand, we discuss signalling molecules that operate primarily in the brain, specifically neuropeptide Y, brain-derived neurotrophic factor and γ-amino butyric acid, that are disturbed by microbial factors, obesity and diabetes and are relevant to mental illness. Finally, we address the usefulness of diet-related interventions to suspend the deleterious relationship between diabesity and mood disorders.
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The Effects of Physical Activity on the Gut Microbiota and the Gut-Brain Axis in Preclinical and Human Models: A Narrative Review.
Increasing evidence supports the importance of the gut microbiota (GM) in regulating multiple functions related to host physical health and, more recently, through the gut-brain axis (GBA), mental health. Similarly, the literature on the impact of physical activity (PA), including exercise, on GM and GBA is growing. Therefore, this narrative review summarizes and critically appraises the existing literature that delves into the benefits or adverse effects produced by PA on physical and mental health status through modifications of the GM, highlighting differences and similarities between preclinical and human studies. The same exercise in animal models, whether performed voluntarily or forced, has different effects on the GM, just as, in humans, intense endurance exercise can have a negative influence. In humans and animals, only aerobic PA seems able to modify the composition of the GM, whereas cardiovascular fitness appears related to specific microbial taxa or metabolites that promote a state of physical health. The PA favors bacterial strains that can promote physical performance and that can induce beneficial changes in the brain. Currently, it seems useful to prioritize aerobic activities at a moderate and not prolonged intensity. There may be greater benefits if PA is undertaken from a young age and the effects on the GM seem to gradually disappear when the activity is stopped. The PA produces modifications in the GM that can mediate and induce mental health benefits.
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Gut microbiota-driven metabolites modulate the development of stress-related mental disorders.
Stress-related mental disorders, including depression, anxiety, and post-traumatic stress disorder, represent a major global health burden, yet their underlying biological mechanisms and effective therapeutic strategies remain incompletely understood. Growing evidence from both preclinical and clinical studies indicates that alterations in gut microbiota composition and function are closely associated with the onset and progression of these disorders. A central role of the gut microbiota is the biotransformation of dietary and host-derived substrates into diverse metabolites that enter systemic circulation and influence host physiology. In this review, we highlight gut microbiota-driven metabolites. short-chain fatty acids, amino acid-related metabolites, bile acids, and monoamine-related metabolites, as key mediators of gut-brain communication that influence neural, immune, epigenetic, and endocrine processes involved in stress-related mental disorders. We summarize emerging microbial and metabolic signatures identified in animal models and human studies. Furthermore, we discuss microbiome-targeted strategies for the prevention and treatment. However, the complexity of the gut microbiota and pronounced inter-individual variability limit causal inference from current clinical studies. Consequently, translating these findings into clinical practice will require standardized study designs, longitudinal clinical investigations, and the integration of multi-omics approaches to advance precision microbiome-based interventions for psychiatric disorders.
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Social anxiety disorder-associated gut microbiota increases social fear.
Social anxiety disorder (SAD) is a crippling psychiatric disorder characterized by intense fear or anxiety in social situations and their avoidance. However, the underlying biology of SAD is unclear and better treatments are needed. Recently, the gut microbiota has emerged as a key regulator of both brain and behaviour, especially those related to social function. Moreover, increasing data supports a role for immune function and oxytocin signalling in social responses. To investigate whether the gut microbiota plays a causal role in modulating behaviours relevant to SAD, we transplanted the microbiota from SAD patients, which was identified by 16S rRNA sequencing to be of a differential composition compared to healthy controls, to mice. Although the mice that received the SAD microbiota had normal behaviours across a battery of tests designed to assess depression and general anxiety-like behaviours, they had a specific heightened sensitivity to social fear, a model of SAD. This distinct heightened social fear response was coupled with changes in central and peripheral immune function and oxytocin expression in the bed nucleus of the stria terminalis. This work demonstrates an interkingdom basis for social fear responses and posits the microbiome as a potential therapeutic target for SAD.