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It is becoming increasingly evident that bidirectional signalling exists between the gastrointestinal tract and the brain, often involving the gut microbiota. This relationship, commonly dubbed the gut–brain axis (or the microbiota–gut–brain axis), involves various afferent and efferent pathways such as the vagus nerve and the hypothalamic-pituitary-adrenal pathway to regulate aspects of homeostasis such as satiety and hunger, and inflammation. Disruption of the gut–brain axis has been shown to be involved in the pathogenesis of a diverse range of diseases, including Parkinson disease and irritable bowel syndrome. This emerging area of research is evolving quickly.
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In this study, the authors show that host microbiota play a key role in modulating microglia homeostasis. Germ-free mice or mice with only limited microbiota complexity displayed defects in microglial cell proportions and maturation, leading to impaired innate immune responses. The authors find that short-chain fatty acid signaling regulates these effects in vivo.
Alterations in the gut microbiota affect stroke outcomes via modulation of T cells, suggesting a gut-brain axis linking commensal microbes with the CNS.
Increased acetate production by an altered gut microbiota in rats fed a high-fat diet activates the parasympathetic nervous system, which in turn promotes increased insulin secretion, increased food intake, obesity and related changes.
Bidirectional gut–brain communications are proving key to both gastrointestinal and neurological diseases. This Review explores the role of the mucosal immune system as gatekeeper and master regulator of these brain–gut and gut–brain communications.
Magarian Blander and colleagues review the effects of the microbiome on innate and adaptive immunological players and how microbiota-derived bioactive molecules affect inflammation and the host response to infection, vaccination and cancer.
The enteric nervous system is vital for life, and its dysfunction participates not only in digestive disorders, but also in diseases of the central nervous system (CNS). Here, Rao and Gershon discuss the gastrointestinal consequences of neurological disorders, the acquisition of CNS disease in the gut and the spread of pathology along the gut–brain axis.
Increasing evidence suggests that Alzheimer disease (AD) is not simply a CNS disorder, but involves interactions between systemic and brain-related factors. Wang and colleagues review the role of amyloid-β (Aβ) in AD, highlighting systemic abnormalities linked to Aβ metabolism and discussing how these abnormalities might influence central pathways of Aβ production and clearance.
Functional urological disorders, like their gastrointestinal counterparts, are interrelated and characterized by a chronic course and treatment resistance. Poor outcomes might be attributable to underlying psychological and psychiatric disorders, as the co-occurrence of functional disorders with mood and anxiety disorders is common. In this Review, the authors describe the hypothetical bladder–gut–brain axis, and explain how it is a useful framework under which this interaction can be studied.
In this Perspective, Suez and Elinav describe the potential for therapeutic approaches based on the use of metabolites secreted, modulated or degraded by the gut microbiome, and issues that will be critical for their implementation.
Here, Patrice Cani and colleagues discuss interactions between gut microorganisms, the endocannabinoid system and host metabolism, in the context of both physiology and pathophysiology. The authors highlight the importance of gut barrier function by discussing the role of specific factors involved in intestinal permeability and their role in the gut microbiota–endocannabinoid system axis. The therapeutic potential of targeting the endocannabinoid system to treat cardiometabolic disorders and intestinal inflammation is also discussed.
Functional dyspepsia is a functional gastrointestinal disorder characterized by discomfort or pain in the upper abdomen (generally associated with food intake) with no apparent underlying organic cause. The three subtypes of functional dyspepsia are postprandial distress syndrome, epigastric pain syndrome and a subtype with mixed features.