Evidence supporting the microbiota-gut-brain axis in a songbird.
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ABSTRACT:
SUBMITTER: Slevin MC
PROVIDER: S-EPMC7728682 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:The gut-brain axis is increasingly recognized as an important pathway of communication and of physiological regulation, and gut microbiota seems to play a significant role in this mutual relationship. Oxidative stress is one of the most important pathogenic mechanisms for both neurodegenerative diseases, such as Alzheimer's or Parkinson's, and acute conditions, such as stroke or traumatic brain injury. A peculiar microbiota type might increase brain inflammation and reactive oxygen species levels and might favor abnormal aggregation of proteins. Reversely, brain lesions of various etiologies result in alteration of gut properties and microbiota. These recent hypotheses could open a door for new therapeutic approaches in various neurological diseases.
| S-EPMC6304899 | biostudies-other
Project description:Disturbances along the brain-gut-microbiota axis may significantly contribute to the pathogenesis of neurodegenerative disorders. Alzheimer's disease (AD) is the most frequent cause of dementia characterized by a progressive decline in cognitive function associated with the formation of amyloid beta (A?) plaques and neurofibrillary tangles. Alterations in the gut microbiota composition induce increased permeability of the gut barrier and immune activation leading to systemic inflammation, which in turn may impair the blood-brain barrier and promote neuroinflammation, neural injury, and ultimately neurodegeneration. Recently, A? has also been recognized as an antimicrobial peptide participating in the innate immune response. However, in the dysregulated state, A? may reveal harmful properties. Importantly, bacterial amyloids through molecular mimicry may elicit cross-seeding of misfolding and induce microglial priming. The A? seeding and propagation may occur at different levels of the brain-gut-microbiota axis. The potential mechanisms of amyloid spreading include neuron-to-neuron or distal neuron spreading, direct blood-brain barrier crossing or via other cells as astrocytes, fibroblasts, microglia, and immune system cells. A growing body of experimental and clinical data confirms a key role of gut dysbiosis and gut microbiota-host interactions in neurodegeneration. The convergence of gut-derived inflammatory response together with aging and poor diet in the elderly contribute to the pathogenesis of AD. Modification of the gut microbiota composition by food-based therapy or by probiotic supplementation may create new preventive and therapeutic options in AD.
| S-EPMC6326209 | biostudies-literature
Project description:BackgroundThe complexity of the pathogenic mechanisms underlying neurodegenerative disorders such as Parkinson's disease (PD) is attributable to multifactorial changes occurring at a molecular level, influenced by genetics and environmental interactions. However, what causes the main hallmarks of PD is not well understood. Recent data increasingly suggest that imbalances in the gut microbiome composition might trigger and/or exacerbate the progression of PD.ObjectiveThe present review aims to (1) report emerging literature showing changes in microbiota composition of PD patients compared to healthy individuals and (2) discuss how these changes may initiate and/or perpetuate PD pathology.MethodsWe analyzed 13 studies published from 2015 and included in this review. Altered microbial taxa were compiled in a detailed table summarizing bacterial changes in fecal/mucosal samples. The methodology was systematically reviewed across the articles and was also included in a table to facilitate comparisons between studies.ResultsMultiple studies found a reduction in short-chain fatty-acid-producing bacteria that can rescue neuronal damage through epigenetic mechanisms. Overall, the studies showed that changes in the gut microbiota composition might influence colonic inflammation, gut permeability, and α-synuclein aggregation, contributing to the neurogenerative process.ConclusionFurther studies with larger cohorts and high-resolution sequencing methods are required to better define gut microbiota changes in PD. Furthermore, additional longitudinal studies are required to determine the causal link between these changes and PD pathogenesis as well as to study the potential of the intestinal microbiota as a biomarker.
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Project description:AimsThe purpose of this review is to explore the interconnected pathways of the microbiota-gut-brain axis (MGBA), focusing on the roles of the vagus nerve and glucagon like peptide-1 in appetite control, and in the development of obesity and diabetes.MethodsType 2 diabetes mellitus (T2DM) and obesity are metabolic disorders whose prevalence has significantly increased in recent decades and is expected to increase every year, to pandemic proportions. These two pathologies often coexist and have substantial public health implications. The term "diabesity" defines the pathophysiological connection between overweight and T2DM. The gut microbiota affects many aspects of the host. Beyond the regulation of intestinal functions and the activation of immune responses, the gut microbiota plays a role in central nervous system functions (i.e., mood, and psychiatric conditions associated with stress and memory) and is a central regulator of metabolism and appetite.ResultsThe MGBA involves pathways such as the autonomic and enteric nervous systems, the hypothalamic- pituitary-adrenal axis, the immune system, enteroendocrine cells, and microbial metabolites. Notably, the vagus nerve plays an essential role in eating behavior by modulating appetite and learning nutritional preferences.ConclusionsBecause of its enteroendocrine cell-mediated interaction with the gut microbiota, the vagus nerve may provide a potential pathway through which gut microorganisms influence host feeding behavior and metabolic control of physiological and pathological conditions.
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Project description:Different bacterial families colonize most mucosal tissues in the human organism such as the skin, mouth, vagina, respiratory, and gastrointestinal districts. In particular, the mammalian intestine hosts a microbial community of between 1,000 and 1,500 bacterial species, collectively called "microbiota." Co-metabolism between the microbiota and the host system is generated and the symbiotic relationship is mutually beneficial. The balance that is achieved between the microbiota and the host organism is fundamental to the organization of the immune system. Scientific studies have highlighted a direct correlation between the intestinal microbiota and the brain, establishing the existence of the gut microbiota-brain axis. Based on this theory, the microbiota acts on the development, physiology, and cognitive functions of the brain, although the mechanisms involved have not yet been fully interpreted. Similarly, a close relationship between alteration of the intestinal microbiota and the onset of several neurological pathologies has been highlighted. This review aims to point out current knowledge as can be found in literature regarding the connection between intestinal dysbiosis and the onset of particular neurological pathologies such as anxiety and depression, autism spectrum disorder, and multiple sclerosis. These disorders have always been considered to be a consequence of neuronal alteration, but in this review, we hypothesize that these alterations may be non-neuronal in origin, and consider the idea that the composition of the microbiota could be directly involved. In this direction, the following two key points will be highlighted: (1) the direct cross-talk that comes about between neurons and gut microbiota, and (2) the degree of impact of the microbiota on the brain. Could we consider the microbiota a valuable target for reducing or modulating the incidence of certain neurological diseases?
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| S-EPMC6646086 | biostudies-literature
Project description:The human gastrointestinal tract is populated with a diverse microbial community. The vast genetic and metabolic potential of the gut microbiome underpins its ubiquity in nearly every aspect of human biology, including health maintenance, development, aging, and disease. The advent of new sequencing technologies and culture-independent methods has allowed researchers to move beyond correlative studies toward mechanistic explorations to shed light on microbiome-host interactions. Evidence has unveiled the bidirectional communication between the gut microbiome and the central nervous system, referred to as the "microbiota-gut-brain axis". The microbiota-gut-brain axis represents an important regulator of glial functions, making it an actionable target to ameliorate the development and progression of neurodegenerative diseases. In this review, we discuss the mechanisms of the microbiota-gut-brain axis in neurodegenerative diseases. As the gut microbiome provides essential cues to microglia, astrocytes, and oligodendrocytes, we examine the communications between gut microbiota and these glial cells during healthy states and neurodegenerative diseases. Subsequently, we discuss the mechanisms of the microbiota-gut-brain axis in neurodegenerative diseases using a metabolite-centric approach, while also examining the role of gut microbiota-related neurotransmitters and gut hormones. Next, we examine the potential of targeting the intestinal barrier, blood-brain barrier, meninges, and peripheral immune system to counteract glial dysfunction in neurodegeneration. Finally, we conclude by assessing the pre-clinical and clinical evidence of probiotics, prebiotics, and fecal microbiota transplantation in neurodegenerative diseases. A thorough comprehension of the microbiota-gut-brain axis will foster the development of effective therapeutic interventions for the management of neurodegenerative diseases.
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Project description:Purpose of reviewAlthough gut microbiota have been associated with the etiology of some diseases, the influence of foods on gut microbiota, especially among pregnant women, remains unclear. Hence, a systematic review was performed to investigate the association between diet and gut microbiota and their influence on metabolic health in pregnant women.Recent findingsWe performed the systematic review using the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) 2020 protocol to investigate the association between diet and gut microbiota and their influence on metabolic role in pregnant women. Five databases were searched for relevant peer-reviewed articles published in English since 2011. Two-staged screening of 659 retrieved records resulted in the inclusion of 10 studies. The collated findings suggested associations between nutrient intakes and four key microbes: Collinsella, Lachnospira, Sutterella, Faecalibacterium, and the Firmicutes/Bacteroidetes ratio in pregnant women. Dietary intakes in pregnancy were found to modify the gut microbiota and positively influence the cell metabolism in pregnant women. This review, however, emphasizes the importance of conducting well-designed prospective cohorts to investigate the role of changes in dietary intakes within the pregnancy and the influence of such changes on gut microbiota.
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Project description:Emerging evidence suggests that gut-brain-microbiota axis (GBMAx) may play a pivotal role linking gastrointestinal and neuronal disease. In this review, we summarize the latest advances in studies of GBMAx in inflammatory bowel disease (IBD) and ischemic stroke. A more thorough understanding of the GBMAx could advance our knowledge about the pathophysiology of IBD and ischemic stroke and help to identify novel therapeutic targets via modulation of the GBMAx.
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Project description:Gut microbiota play an important role in maintaining intestinal health and are involved in the metabolism of carbohydrates, lipids, and amino acids. Recent studies have shown that the central nervous system (CNS) and enteric nervous system (ENS) can interact with gut microbiota to regulate nutrient metabolism. The vagal nerve system communicates between the CNS and ENS to control gastrointestinal tract functions and feeding behavior. Vagal afferent neurons also express receptors for gut peptides that are secreted from enteroendocrine cells (EECs), such as cholecystokinin (CCK), ghrelin, leptin, peptide tyrosine tyrosine (PYY), glucagon-like peptide-1 (GLP-1), and 5-hydroxytryptamine (5-HT; serotonin). Gut microbiota can regulate levels of these gut peptides to influence the vagal afferent pathway and thus regulate intestinal metabolism via the microbiota-gut-brain axis. In addition, bile acids, short-chain fatty acids (SCFAs), trimethylamine-N-oxide (TMAO), and Immunoglobulin A (IgA) can also exert metabolic control through the microbiota-gut-liver axis. This review is mainly focused on the role of gut microbiota in neuroendocrine regulation of nutrient metabolism via the microbiota-gut-brain-liver axis.
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