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Gut Microbiota and Neurologic Diseases and Injuries.
The brain-gut axis is a bidirectional communication pathway connecting the central nervous system (CNS) and the gastrointestinal tract via nerve transmission, hormone, immune system, and other molecular signals. The bacterial flora of the human gut contributes direct and indirect signals to the CNS along the brain-gut axis. Alterations in gut flora, a state known as dysbiosis, has been tied to systemic inflammation, increased bacterial translocation, and increased absorbance of microbial by-products. An increase in recent literature has highlighted the role of the gut-brain axis in CNS pathology. This chapter reviews the association between gut flora dysbiosis and disorders of the central nervous system including autoimmune disease, developmental disorders, physiologic response to traumatic injury, and neurodegenerative disease.
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Transcriptional markers of excitation-inhibition balance in germ-free mice show region-specific dysregulation and rescue after bacterial colonization.
BACKGROUND: Studies of germ-free (GF) mice demonstrate that gut microbiota can influence behaviour by modulating neurochemical pathways in the brain, and that bacterial colonization normalizes behavioural deficits in GF-mice. Since disrupted GABAergic and glutamatergic signaling are reported in mood disorders, this study investigated the effect of gut microbiota manipulations on EIB-relevant gene expression in the brain. METHODS: GF Swiss-Webster mice were colonized with E. coli JM83, complex microbiota (specific-pathogen-free; SPF), or no microbiota, and compared with controls (n = 6/group). 21 synaptic genes representing GABAergic, glutamatergic, BDNF, and astrocytic functions were measured in the hippocampus, amygdala, and prefrontal cortex using quantitative PCR. Gene co-expression analysis was used to identify gene modules related to colonization status, and compared by permutation analysis. Gene expression profiles were compared to existing post-mortem cohorts of depressed subjects (n = 28 cases vs 28 controls). RESULTS: Region-specific alterations in gene expression were observed in GF-mice compared to controls. 58% of all genes (14/24) altered in GF-mice were normalized following SPF-colonization. GF-mice displayed disorganization of gene co-expression networks in all three brain regions (hippocampus, p = 0.0003; amygdala, p = 0.0012; mPFC, p = 0.0069), which was restored by SPF colonization in hippocampus (p v.s. GF = 0.0003, p v.s. control = 0.60). The hippocampal gene expression profile in GF-mice was significantly correlated with that in human depression (ρ = 0.51, p = 0.027), and this correlation was not observed after colonization. CONCLUSION: Together, we show that the absence of gut microbiota disrupts the expression of EIB-relevant genes in mice, and colonization restores EIB-relevant expression, in ways that are relevant to human depression.
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Exploring the effect of prenatal maternal stress on the microbiomes of mothers and infants: A systematic review.
Prenatal maternal stress (PNMS)-characterized by exposure to stress, anxiety, depression, or intimate partner violence-has been linked to biological alterations in infants, including disruptions to their intestinal microbiota, which have long-term implications for children's developmental outcomes. Significant research has been done examining the effects of PNMS on the microbiome in animals, but less is known about these effects in human research. The current systematic review aimed to synthesize current findings on the association between PNMS and mother and infant microbiomes. Medline, Embase, PsycInfo, Web of Science, and Eric databases were searched through to February 2022. A total of eight studies (n = 2219 infants, 2202 mothers) were included in the qualitative synthesis. Findings provided promising evidence of the role that PNMS plays in altering the microbial composition, diversity, and gut immunity in mothers and infants. Notably, majority of included studies found that higher PNMS was linked to increases in genera from the phylum Proteobacteria. The factors influencing these effects are explored including nutrition, birth mode, and parenting behaviors. Potential interventions to mitigate the adverse effects of PNMS are discussed, along with recommendations for future studies with longitudinal designs to better understand the appropriate type and timing of interventions needed to promote "healthy" maternal and infant microbial functioning.
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Long-term exposure to polystyrene microplastics reduces macrophages and affects the microbiota-gut-brain axis in mice.
The remarkably increase in plastic use has led to worldwide pollution involving microplastics (MPs), which have been shown to be potentially hazardous substances. Although several studies have focused on the effects of small MPs on the brain and behavior of aquatic species, their effects on the mouse brain and the underlying mechanisms remain unclear. Our study's aim was to investigate the effects of long-term oral ingestion of different sizes of MPs (0.1, 5, and 50 μm) on mouse colon tissue. Of these sizes, the smallest (0.1 μm) had the greatest effect. Pre-administration of MP promotes colitis but reduces tumor growth in a colitis-associated colorectal cancer (CAC) mouse mode. MPs can increase inflammation in mice via activation of the very late antigen 4-vascular cell adhesion molecule 1 (VLA4-VCAM1) signaling pathway in macrophages, while also inducing macrophage reduction in the late phase of inflammation. In the microbiota-gut-brain axis, polystyrene MP treatment altered bile acid and carbohydrate metabolism in the intestine, inhibited intestinal motility, reduced water reabsorption, and led to a certain degree of depression in mice. These findings suggest that small MPs can induce macrophage reduction, thereby affecting the physical and mental health by modulating the microbiota-gut-brain axis.
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An overview of the effect of probiotics and exercise on mood and associated health conditions.
The present paper provides a review of the current knowledge relating to the health benefits of probiotics, specially focused on the effects they may have together with physical exercise on mood disorders and related chronic medical conditions.With both these conditions being a substantial contributor to the global disease burden, any alternative therapy must be considered. Probiotics influence the gut microbiota through a complex network of events which can influence mechanisms leading to development of mood disorders such as depression and anxiety. Similarly, through a complex interaction between psychological and neurobiological mechanisms, exercise has been found to play a key role in mood enhancement.
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The microbiome as a novel paradigm in studying stress and mental health.
At the intersection between neuroscience, microbiology, and psychiatry, the enteric microbiome has potential to become a novel paradigm for studying the psychobiological underpinnings of mental illness. Several studies provide support for the view that the enteric microbiome influences behavior through the microbiota-gut-brain axis. Moreover, recent findings are suggestive of the possibility that dysregulation of the enteric microbiota (i.e., dysbiosis) and associated bacterial translocation across the intestinal epithelium may be involved in the pathophysiology of stress-related psychiatric disorders, particularly depression. The current article reviews preliminary evidence linking the enteric microbiota and its metabolites to psychiatric illness, along with separate lines of empirical inquiry on the potential involvement of psychosocial stressors, proinflammatory cytokines and neuroinflammation, the hypothalamic-pituitary-adrenal axis, and vagal nerve activation, respectively, in this relationship. Finally, and drawing on these independent lines of research, an integrative conceptual model is proposed in which stress-induced enteric dysbiosis and intestinal permeability confer risk for negative mental health outcomes through immunoregulatory, endocrinal, and neural pathways. (PsycINFO Database Record
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Pathophysiology of Functional Gastrointestinal Disorders: A Holistic Overview.
Background and Summary: Traditionally, functional gastrointestinal disorders (FGID), including functional dyspepsia or irritable bowel syndrome (IBS), are defined by more or less specific symptoms and the absence of structural or biochemical abnormalities that cause these symptoms. This concept is now considered to be outdated; if appropriate tests are applied, structural or biochemical abnormalities that explain or cause the symptoms may be found in many patients. Another feature of FGID are the highly prevalent psychiatric comorbidities, such as depression and anxiety. It is implied that mood disorders "cause" gastrointestinal symptoms. In fact, epidemiological data now provide strong evidence that in subsets of cases, gastrointestinal (GI) symptoms arise first and mood disorders occur later, while in other patients the reverse appears to happen. Possible mechanisms for gut-brain dysfunction have been identified, with systemic minimal inflammation as a causal factor in at least some subjects. Other mechanisms that play a role in FGID include chronic infections, intestinal microbiota, low-grade mucosal inflammation including the increase of eosinophils, systemic immune activation, altered intestinal permeability, in diarrhea predominant IBS altered bile salt metabolism, abnormalities in the serotonin metabolism and genetic factors. All these factors might be modulated by environmental factors such as diet. Key Messages: While a number of factors can be linked to specific symptoms (e.g., pain or diarrhea), it is evident that the symptom-based categorization of patients will not allow targeted treatments that specifically address the underlying pathophysiology.
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Modulation of Gut-Brain Axis by Probiotics: A Promising Anti-depressant Approach.
The human digestive system is embedded with trillions of microbes of various species and genera. These organisms serve several purposes in the human body and exist in symbiosis with the host. Their major role is involved in the digestion and conversion of food materials into many useful substrates for the human body. Apart from this, the gut microbiota also maintains healthy communication with other body parts, including the brain. The connection between gut microbiota and the brain is termed as gut-brain axis (GBA), and these connections are established by neuronal, endocrine and immunological pathways. Thus, they are involved in neurophysiology and neuropathology of several diseases like Parkinson's disease (PD), Alzheimer's disease (AD), depression, and autism. There are several food supplements such as prebiotics and probiotics that modulate the composition of gut microbiota. This article provides a review about the role of gut microbiota in depression and supplements such as probiotics that are useful in the treatment of depression.
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Pleiotropic modulation of the gut-brain-lung axis by ketamine and its enantiomers.
Ketamine, a potent N-methyl-D-aspartate receptor (NMDAR) antagonist, is widely used for anesthesia and analgesia and, because of its rapid antidepressant effects, in psychiatry. Increasing evidence suggests that ketamine and its enantiomers-(R)-ketamine (arketamine) and (S)-ketamine (esketamine)-also modulate systemic immunity and provide organ protection, partly through interactions with the gut microbiota, microbial metabolites, and intestinal immune-cell trafficking. However, these gut-mediated pathways must be distinguished from ketamine's well-established direct central and peripheral actions. In this review, we summarize how ketamine engages the gut-brain and gut-lung axes, emphasizing anti-inflammatory, immunoregulatory, and barrier-protective effects, while critically evaluating the evidence for causality in gut-organ communication. Along the gut-brain axis, ketamine is associated with restoration of microbial balance, normalization of short-chain fatty acid levels, and reduced migration of gut-derived γδ T17 and Th17 cells to the central nervous system, correlating with attenuated neuroinflammation and depressive-like behaviors. Through the gut-lung axis, ketamine has been reported to limit bacterial translocation and mesenteric lymph-associated inflammatory signaling and reduces pulmonary infiltration of pro-inflammatory cells, suggesting potential relevance in acute lung injury and other respiratory disorders. We also discuss enantiomer-specific effects: arketamine appears to provide more sustained neuroprotection and may be associated with fewer adverse effects than esketamine. Overall, these findings suggest the broad therapeutic potential of ketamine and its enantiomers for neuropsychiatric and inflammatory diseases, while underscoring the need for careful evaluation of long-term safety, optimal dosing, microbiota-targeted adjunctive strategies, and causal studies to distinguish direct pharmacological actions from indirect, microbiota-mediated effects.
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Relevance of gutmicrobiota in cognition, behaviour and Alzheimer's disease.
Approximately 95% of the symbiotic microbes in human body are located in the gut. This microbioma is involved in important homeostatic processes, not only related to gastrointestinal function but also to several complex modulatory processes, such as glucose and bone metabolism, inflammation and immune response, peripheral (enteric) and central neurotransmission. For that reason, recent studies proposed that abnormalities in gut microbiota may play a role in systemic and central nervous system (CNS) conditions. Therefore, the integrity of gut microbiota be relevant to the pathophysiology and control of important medical diseases like diabetes mellitus, inflammatory and autoimmune diseases, and even neuropsychiatric disorders such as depression, autism spectrum disorder, Parkinson's and Alzheimer disease. Gut microbiota may affect brain function and behaviour through the microbiota-gut-brain axis, in bidirectional interplay with top-down and bottom-up regulations. Through metabolic activity of non- pathogenical microorganisms and secretion of functional by-products that increase the permeability of the intestinal mucosa, the gut microbiota influences both the production and absorption of neurotransmitters (e.g., serotonin and GABA), increasing their bioavailability to the CNS. It has been further shown some components of the gut microbiota - predominantly bacteria - synthesize and release amyloid peptides and lipopolysaccharides, which in turn activate inflammatory signalling through the release of cytokines, with potential effects on the pathophysiological cascade of Alzheimer disease.