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Effects of 'Healthy' Fecal Microbiota Transplantation against the Deterioration of Depression in Fawn-Hooded Rats.
Depression is a recurrent, heterogeneous mood disorder occurring in more than 260 million people worldwide. Gut microbiome dysbiosis is associated with the development of depressive-like behaviors by modulating neuro-biochemical metabolism through the microbiome-gut-brain (MGB) axis. Fecal microbiota transplantation (FMT) has been proposed as a potential therapeutic solution for depression, but the therapeutic efficiency and mechanism are unknown. Here, we performed an FMT from Sprague-Dawley (SD) rats ('healthy' controls) to Fawn-hooded (FH) rats (depression model). Pre-FMT, the FH rats exhibited significantly elevated depressive-like behaviors and distinct neurotransmitter and cytokine levels compared with SD rats. Post-FMT, FH recipients receiving FH fecal microbiota (FH-FH rats) showed aggravated depressive-like behaviors, while the ones receiving SD microbiota (FH-SD rats) had significantly alleviated depressive symptoms, a significant increase in hippocampal neurotransmitters, and a significant decrease of some hippocampal cytokines than FH-FH rats. SD-FMT resulted in the FH-SD rats' gut microbiome resembling the SD donors, and a significant shift in the serum metabolome but not the hippocampal metabolome. Co-occurrence analysis suggests that SD-FMT prevented recipients' depression development via the significant decrease of gut microbial species such as Dialister sp., which led to the recipients' metabolic modulation in serum and hippocampus through the enteric nervous system, the intestinal barrier, and the blood-brain barrier. Our results provided new data pointing to multiple mechanisms of interaction for the impact of gut microbiome modulation on depression therapy. IMPORTANCE Depression is a chronic, recurrent mental disease, which could make the patients commit suicide in severe cases. Considering that gut microbiome dysbiosis could cause depressive symptoms in animals through the MGB axis, the modification of gut microbiota is expected to be a potential therapy for depression, but the daily administration of probiotics is invalid or transient. In this study, we demonstrated that the gut microbiome transferred from a healthy rat model to a depressive rat model could regulate the recipient's neurobiology and behavior via the systematic alternation of the depressive gut microbiota followed by the serum and hippocampal metabolism. These results underline the significance of understanding the impact of gut microbiota on mental disorders and suggest that 'healthy' microbiota transplantation with the function to solve the host's cerebral inflammation may serve as a novel therapeutic strategy for depression.
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The Intestinal Microbiota in the Irritable Bowel Syndrome.
The irritable bowel syndrome (IBS) is a chronic abdominal symptom complex occurring in a bowel devoid of discernible relevant pathology. There is growing interest in the role of the intestinal microbiota as a basis for the intestinal and possibly behavioral manifestations of this condition. Molecular-based microbial profiling has revealed compositional changes in the microbiota of at least a subset of IBS patients but the data are often conflicting and no microbial signature for this condition has yet been defined. Animal studies in which a previously stable intestinal microbiota is perturbed, by antibiotics or dietary change, results in alterations in intestinal function reminiscent of that seen in IBS patients. These include visceral sensitivity to painful stimuli, altered motility and intestinal barrier function as well as immune activation, and low-grade inflammation. More recent studies have shown that perturbation of the microbial composition of the gut alters brain chemistry and behavior. In a step toward establishing a causal link between an altar microbiota and gut-brain manifestations of IBS, colonization of germ-free mice with microbiota from IBS patients results in an IBS-like phenotype, including alterations and behavior if the donor exhibited psychiatric comorbidity, such as high levels of anxiety. This model provides an opportunity for exploring the mechanisms underlying host-microbe interactions relevant to the pathogenesis of IBS and for developing novel therapeutic targets.
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Exploring the Link Between the Gut Microbiota and Epigenetic Factors in Anorexia Nervosa.
OBJECTIVE: Anorexia nervosa (AN) is an often chronic eating disorder that involves genetic, neurohormonal, and epigenetic factors along with key contributions from the microbiota-gut-brain axis. However, interactions between these factors are poorly understood. Recent studies have emphasized the microbiota-gut-brain axis and epigenetic changes as potentially important contributors to AN. Exploring these interactions may improve understanding of the etiology and persistence of AN. METHODS: Studies specifically addressing microbial-epigenetic interactions in AN remain limited. However, similar associations have been documented in related disorders such as obesity and depression, providing potential models for AN research. RESULTS: Research in obesity has shown that dietary factors influence the composition of the gut microbiota and subsequent epigenetic modifications, affecting metabolic parameters and disease progression. Similarly, in depression, microbially produced metabolites influence brain function and epigenetic processes, contributing to neuropsychiatric symptoms. In AN, altered microbial composition may affect weight regulation and epigenetic patterns. Therapies targeting the microbiome, such as fecal microbiota transplantation, are under investigation for AN, highlighting the potential therapeutic utility of ameliorating microbial dysbiosis. DISCUSSION: This article highlights the importance of investigating microbial-epigenetic interactions in AN. By drawing parallels with obesity and depression, we aim to deepen our understanding of AN mechanisms and ultimately improve patient outcomes.
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Enteric nervous system and intestinal epithelial regulation of the gut-brain axis.
The gut-brain axis describes a bidirectional interplay within the enteric environment between the intestinal epithelium, the mucosal immune system, and the microbiota with the enteric nervous system. This interplay provides a link between exogenous environmental stimuli such as nutrient sensing, and nervous system function, as well as a mechanism of feedback from cortical and sensory centers of the brain to enteric activities. The intestinal epithelium is one of the human body's largest sources of hormones and neurotransmitters, which have critical effects on neuronal function. The influence of the gut microbiota on these processes appears to be profound; yet to date, it has been insufficiently explored. Disruption of the intestinal microbiota is linked not only to diseases in the gut but also to brain symptomatology, including neurodegenerative and behavioral disorders (Parkinson disease, Alzheimer disease, autism, and anxiety and/or depression). In this review we discuss the cellular wiring of the gut-brain axis, with a particular focus on the epithelial and neuronal interaction, the evidence that has led to our current understanding of the intestinal role in neurologic function, and future directions of research to unravel this important interaction in both health and allergic disease.
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[The abdominal brain: neuroanatomic perspectives for the abdominal surgeon].
The "abdominal brain" does not only consist of a separate enteric nervous system but also of bidirectional connections to the autonomous nerve system with parasympathicus und sympathicus as well as brain and spinal cord. Novel studies have shown that these connections can quickly transfer information on the ingested nutrients to the brain to conduct the feeling of hunger and more complex behaviour, such as "reward-related learning". However, even emotional experience, in particular, stress, has a strong impact onto the gastrointestinal system. The immune system, motility and barrier function of the gastrointestinal tract are modulated by the intestinal microbiota. Local bacteria may directly influence neuronal communication by released metabolic products and neuropeptides as well as may control inflammatory factors. Intensive research over the last 10 years was able to provide evidence that intestinal microbiota may affect emotional and cognitive aspects of our behaviour and, thus, it might be in the focus of numerous neuropsychiatric diseases, such as depressions and anxiety disorders.The presented review is to provide a short summary of the I): anatomic basics of the so-called gut-brain axis and II): modi of the bidirectional regulation. Through indirect connections to the limbic system, gut-brain axis can substantially influence stress and anxiety but also the pain processing. In addition, the role of microbiota is outlined and future paths are shown, e.g., how the (microbiota-)gut-brain axis may alter emotional experience, pain processing and intestinal function. Such associations are relevant for further development of visceral medicine, and, thus, also for the abdominal surgeon to derive future treatment concepts with interdisciplinary orientation.
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Antibiotic-induced microbiome depletion is associated with resilience in mice after chronic social defeat stress.
BACKGROUND: The brain-gut axis plays a role in the pathogenesis of stress-related disorders such as depression. However, the role of brain-gut axis in the resilience versus susceptibility after stress remains unclear. Here, we examined the effects of antibiotic-induced microbiome depletion on an anhedonia-like phenotype in adult mice subjected to chronic social defeat stress (CSDS). METHODS: Using CSDS paradigm, we investigated the effects of antibiotic-induced microbiome depletion on the resilience versus susceptibility in mice. RESULTS: Treatment with an antibiotic cocktail for 14 days significantly decreased the diversity and composition of the microbiota in the host gut. Proteobacteria were markedly increased after treatment with the antibiotic cocktail. At the genus and species levels, the antibiotic-treated group exhibited marked alterations in the microbiota compared with a control group. CSDS was shown to significantly improve the abnormal composition of gut microbiota in the antibiotic-treated group. CSDS did not produce an anhedonia-like phenotype in the antibiotic-treated mice, but did induce an anhedonia-like phenotype in control mice, suggesting that gut bacteria are essential for the development of CSDS-induced anhedonia. CSDS treatment did not alter the plasma levels of interleukin-6 or the expression of synaptic proteins, such as PSD-95 and GluA1, in the prefrontal cortex of antibiotic-treated mice. LIMITATIONS: Specific microbiome were not determined. CONCLUSIONS: These findings suggest that antibiotic-induced microbiome depletion contributed to resilience to anhedonia in mice subjected to CSDS. Therefore, it is likely that the brain-gut axis plays a role in resilience versus susceptibility to stress.
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Bioengineered gut bacterium synthesizing levodopa alleviates motor deficits in models of Parkinson's disease.
L-3,4-Dihydroxyphenylalanine (L-DOPA), synthesized from L-tyrosine, is a direct precursor to dopamine. L-DOPA is the gold-standard treatment for Parkinson's disease (PD), given orally alongside decarboxylase inhibitors (e.g., benserazide) to enhance bioavailability. However, its chronic daily pulsatile-like delivery is associated with complications. Herein, we show the construction and in vivo efficacy of a programmable, titratable, genetically engineered E. coli Nissle 1917 system (EcNL-DOPA) that continuously synthesizes L-DOPA from L-tyrosine for systemic distribution. Oral administration of EcNL-DOPA with benserazide maintains therapeutic plasma L-DOPA concentrations and increases brain dopamine levels. EcNL-DOPA improves motor performance and limits depressive-like behaviors without adverse side effects in healthy mice, Parkinsonian mice, and canine models. Simulated physiological models from pharmacokinetic and pharmacodynamic studies in canines demonstrate the translational feasibility of this biotherapeutic system for potential human studies. This work lays the groundwork for EcNL-DOPA as a continuous, non-invasive microbial drug delivery platform for PD and chronic neurological diseases.
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Multimodal (Bio)Markers and Risk of Obesity - A Comprehensive Scoping Review.
Obesity has been associated with several chronic diseases, especially noncommunicable ones and related comorbidities. Despite international efforts to decrease the prevalence of obesity, the number of persons struggling with this ailment is not decreasing. An important aspect is obesity prevention, including the early detection of the risk, i.e. whether an individual is likely to develop obesity, to allow for early risk stratification and countermeasure initiation. However, obesity is a complex and multifactorial complication, and many factors appear to play a role, including age, sex, diet, physical activity (PA), psychological and emotional status, genetic make-up, epigenetics, and gut microbiota. One isolated biomarker, therefore, could not enable optimal risk stratification and prognosis for the individual; rather, a combined set or multimodal approach to tackle risk prediction is demanded. Such a multimodal interpretation would integrate biomarkers from various domains, such as more classical markers (insulin, leptin), multiomics (e.g. genetics, epigenomics, transcriptomics, proteomics, and metabolomics), behavioral attributes (dietary, PA, and sleep patterns, and smoking status), psychological traits (mental health status, depression, and eating disorders), and gut-microbiota (composition and diversity) into a combined interpretation, also employing more advanced interpretation tools, such as machine learning and artificial intelligence. In this scoping review, we aimed to summarize the current state of the art in this area, highlighting the progress and novel approaches in combating obesity, and focusing on the feasibility and effectiveness of such biomarkers and their application within clinical trials. In addition, we outline potential future steps and recommendations for future approaches.
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Melatonin Ameliorates Neuropsychiatric Behaviors, Gut Microbiome, and Microbiota-Derived Metabolites in Rats with Chronic Sleep Deprivation.
With the increasing prevalence of sleep deprivation (SD)-related disorders, the effective treatment of sleep disorders has become a critical health research topic. Thus, we hypothesized and investigated the effectiveness of a 3-week melatonin intervention on neuropsychiatric behavioral responses mediated throughout melatonin receptors, gut microbiota, and lipid metabolites in rats with chronic SD. Eighteen 6-week-old Wistar rats were used and divided into the control grup (C, n = 6), SD group (n = 6), and melatonin-supplemented group (SDM, n = 6). During weeks 0 to 6, animals were provided with the AIN-93M diet and free access to water. Four-week chronic SD was conducted from weeks 7 to 10. Exogenous melatonin administration (10 mg/kg BW) was injected intraperitoneally 1 h before the daily administration of SD for 3 weeks in the SDM group. SD rats exhibited anxiety-like behavior, depression-like behavior, and cognitive impairment. Exogenous melatonin administration ameliorated neuropsychiatric behaviors induced by chronic SD. Analysis of fecal metabolites indicated that melatonin may influence brain messaging through the microbiota-gut-brain axis by increasing the production of short-chain fatty acids (SCFA) and decreasing the production of secondary bile acids (SBA). Four-week SD reduced the cerebral cortex expression of MT1, but not in the colon. Chronic SD led to anxiety and depression-like behaviors and cognitive decline, as well as the reduced intestinal level of SCFAs and the enhanced intestinal level of SBAs in rats. In this work, we confirmed our hypothesis that a 3-week melatonin intervention on neuropsychiatric behavioral response mediated throughout melatonin receptors, gut microbiota, and lipid metabolites in rats with chronic SD.
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Relationship between human oral microbiome dysbiosis and neuropsychiatric diseases: An updated overview.
The role of the gut-brain axis in mental health disorders has been extensively studied. As the oral cavity is the starting point of the digestive tract, the role that the oral microbiota plays in mental health disorders has gained recent attention. Oral microbiota can enter the bloodstream and trigger inflammatory responses or translocate to the brain through the trigeminal nerve or olfactory system. Hence, the concept of the oral microbiota-brain axis has emerged. Several hypotheses have been suggested that the oral microbiota can enter the gastrointestinal tract and affect the gut-brain axis; however, literature describing oral-brain communication remains limited. This review summarizes the characteristics of oral microbiota and its mechanisms associated with mental health disorders. Through a comprehensive examination of the relationship between oral microbiota and various neuropsychiatric diseases, such as anxiety, depression, schizophrenia, autism spectrum disorder, epilepsy, Parkinson's disease, and dementia, this review seeks to identify promising avenues of future research.