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Microbial alpha diversity in the intestine negatively correlated with disease duration in patients with Meniere's disease.
Ménière's disease (MD) is characterized by loss of balance and hearing disorders. Although there is known to be endolymphatic hydrops involved in the pathological process, the pathogenesis of the disease is still largely unclear. Approximately half of patients with MD suffer from depressive symptoms and high levels of several stress hormones were observed in MD and depression, simultaneously. Recently, gut microbes have been shown to influence the function of the central nervous system in humans through their metabolites. We studied the intestinal microbiota of 10 patients with MD and 11 healthy donors (HD). Significant negative correlations were found between disease duration and alpha diversity indexes of gut microbes in patients with MD. The relative abundance of the species Butyricicoccus ambiguous taxa was increased in patients with MD compared with that of HD. In contrast, Oscillospiraceae UCG-002/UCG-005 ambiguous taxa and Anaerovoracaceae (Eubacterium) brachy group uncultured bacterium were increased in the relative abundance of HD than that of patients with MD. The relative abundance of the Butyricicoccus species was positively correlated with disease duration. Thus, these compositional alterations of gut microbes in patients with MD are associated with inner ear pathologies, such as endolymphatic hydrops, by changing the metabolite profiles in the intestine.
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Research Progress on the Regulatory Mechanisms of Gut Microbiota in Methamphetamine Addiction and Targeted Interventions.
Methamphetamine (METH) is a globally prevalent, highly addictive synthetic psychostimulant, for which no FDA-approved pharmacotherapy is currently available for METH use disorder (MUD). The microbiota-gut-brain axis has been well established as a key regulatory pathway in substance use disorders, yet its specific mechanistic basis and translational potential in METH addiction remain to be systematically elucidated. This review synthesizes current preclinical and clinical evidence demonstrating that METH exposure induces profound gut microbiota dysbiosis, characterized by the depletion of beneficial genera such as Faecalibacterium and Lactobacillus, enrichment of proinflammatory phylum Proteobacteria and concurrent dysregulation of microbial metabolites including short-chain fatty acids (SCFAs), tryptophan derivatives and bile acids. These microbial signals mediate bidirectional gut-CNS crosstalk through neuroimmune, neuroendocrine (hypothalamic-pituitary-adrenal (HPA) axis) and vagal pathways, thereby exacerbating the core central pathologies of METH addiction: neurotransmitter system imbalance, neuroinflammation and oxidative stress and dysfunction of addiction-related neural circuits. We further elaborate that gut microbiota-driven epigenetic modifications and transgenerational effects reinforce the persistence and heritability of addictive phenotypes. Importantly, microbiota-targeted interventions, including probiotics, prebiotics, faecal microbiota transplantation (FMT) and dietary modulation, can alleviate METH-induced affective disturbances (anxiety/depression-like behaviours), multiorgan damage (neurotoxicity, reproductive impairment) and relapse risk, via restoring gut microbial homeostasis, repairing intestinal barrier integrity and normalizing gut-brain axis signalling. Collectively, this review positions the gut microbiota as a critical peripheral regulatory node in METH addiction, providing a robust preclinical foundation for the development of gut-brain axis-targeted combination therapies for MUD.
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The influence of endocrine disruptors on the gut microbiota.
Endocrine disruptors (EDs) are closely associated with the second brain, the microbiota-derived enteric nervous system, commonly referred to as the gut microbiota. The microbiota plays a crucial role in human health and the development of diseases. In today's industrialized world, the presence of EDs in air, water, and soil leads to primary human exposure through dermal contact and ingestion. The impact of these EDs on the microbiota remains unclear. EDs that disrupt the balance of the gut microbiota may contribute to a range of disorders, including metabolic (obesity, diabetes mellitus), cardiovascular (vascular stenosis, cerebrovascular disease), reproductive (infertility, ovarian and testicular tumors), neurological (dysfunction of the amygdala, cortex, and cerebellum), and behavioral disorders (dementia, depression, anxiety, and schizophrenia). This review examines the effects of commonly encountered environmental EDs on the gut microbiota and summarizes the most recent findings on this topic. The concept of the microbiota-derived enteric nervous system and the modulation of the hormonal system through interactions between microorganisms and environmental chemicals have prompted specialists in endocrinology and metabolism to reconsider patient management and treatment strategies. This necessitates a comprehensive evaluation of treatment options that incorporate microbiome data. The information presented in this review will help illuminate future research directions and serve as a valuable resource for subsequent studies.
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Early environmental exposure to oxytetracycline in Danio rerio may contribute to neurobehavioral abnormalities in adult zebrafish.
The common antibiotic oxytetracycline (OTC) is nowadays commonly found in natural aquatic environments. However, the underlying mechanisms of low-dose OTC exposure and its neurotoxic effects on aquatic animals remain unknown. In this study, we exposed zebrafish larvae to environmental concentrations of OTC in early life and performed neurobehavioral, 16S rRNA gene sequencing, and transcriptomic analyses. OTC exposure resulted in hyperactivity of larvae and a significant reduction in the number of neurons in the midbrain. The expression levels of 15 genes related to neural function changed. Additionally, the composition of 65 genera of the gut microbiota of larvae was altered, which may be one of the reasons for the abnormal neural development. We further studied the long-term outcomes among adult fish long after cessation of OTC exposure. OTC treatment caused adult fish to be depressive and impulsive, symbolizing bipolar disorder. Adult fish exposed to OTC had significantly fewer neurons and their gut bacteria composition did not recover 104 days after terminating OTC exposure. Finally, we analyzed the correlation between the gut microbiota of larvae, genes related to neural function, and metabolites of adult fish brain tissue. The results showed that the abundance of several members of the biome in larvae was related to the transcription levels of genes related to neural function, which were related to the metabolic levels in the adult brain. In conclusion, our study showed that early-life exposure to environmental concentrations of OTC can lead to persistent neurobehavioral abnormalities until adulthood through dysbiosis in the gut microbiota.
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Special issue on "Brain-body communication in health and diseases".
Bidirectional interaction between the brain and the peripheral organs plays a key role in homeostasis in the body. Abnormalities in brain-body communication potentially leads to a number of brain diseases, including psychiatric and neurodegenerative disorders. For example, dysbiosis of gut microbiota and altered levels of microbes-derived compounds plays an important role in the pathophysiology of a number of psychiatric disorders and neurodegenerative disorders. Furthermore, depression is the most common psychiatric symptom in patients with physical disorders, including pain and cardiovascular diseases. This special issue brings together current information on the brain-body communication in health and diseases.
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Optimized oxygen therapy improves sleep deprivation-induced cardiac dysfunction through gut microbiota.
Adequate sleep is of paramount importance for relieving stress and restoring mental vigor. However, the adverse physiological and pathological responses resulting from sleep insufficiency or sleep deprivation (SD) are becoming increasingly prevalent. Currently, the impact of sleep deficiency on gut microbiota and microbiota-associated human diseases, especially cardiac diseases, remains controversial. Here, we employed the following methods: constructed an experimental sleep-deprivation model in mice; conducted 16S rRNA sequencing to investigate the changes in gut microbiota; through fecal microbiota transplantation (FMT) experiments, transplanted fecal microbiota from sleep-deprived mice to other mice; established an environment with a 30% oxygen concentration to explore the therapeutic effects of oxygen therapy on gut microbiota-associated cardiac fibrosis and dysfunction; and utilized transcriptome data to study the underlying mechanisms of oxygen therapy. The results revealed that: sleep-deprived mice exhibited weakness, depression-like behaviors, and dysfunction in multiple organs. Pathogenic cardiac hypertrophy and fibrosis occurred in sleep-deprived mice, accompanied by poor ejection fraction and fractional shortening. 16S rRNA sequencing indicated that sleep deprivation induced pathogenic effects on gut microbiota, and similar phenomena were also observed in mice that received fecal microbiota from sleep-deprived mice in the FMT experiments. The environment with a 30% oxygen concentration effectively alleviated the pathological impacts on cardiac function. Transcriptome data showed that oxygen therapy targeted several hypoxia-dependent pathways and inhibited the production of cardiac collagen. In conclusion, these results demonstrate the significance of sufficient sleep for gut microbiota and may represent a potential therapeutic strategy, where the oxygen environment exerts a protective effect on insomniacs through gut microbiota.
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When the microbiome helps the brain-current evidence.
The gut microbiota-brain axis has been recognized as a network of connections that provides communication between the gut microflora and both central and autonomic nervous system. The gut microbiota alteration has been targeted for therapy in various neurodegenerative and psychiatric disbalances. Psychobiotics are probiotics that contribute beneficially to the brain function and the host mental health as a result of an interaction with the commensal gut bacteria, although their mechanism of action has not been completely revealed. In this state-of-art review, the findings about the potential therapeutic effects of the psychobiotics alone or in combination with conventional medicine in the treatment of neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease, as well as in some psychiatric diseases like depression, schizophrenia, and bipolar disorder, have been summarized. The evidence of the psychobiotics therapeutic outcomes obtained in preclinical and clinical trials have been given respectively for the observed neurodegenerative and psychiatric disorders.
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Ergothioneine, a metabolite of the gut bacterium Lactobacillus reuteri, protects against stress-induced sleep disturbances.
The relationships between depression and gut microbiota, particularly those involving the immune system, have become a major focus of recent research. Here, we analyzed changes in gut microbiota and their sulfur metabolites in the feces of a depression rat model using the modified 14-day social defeat stress (SDS) paradigm. Our results showed that SDS increased fecal Lactobacillus reuteri in correlation with ergothioneine levels at around day 11, which continued for at least 1 month following SDS administration. In vitro study further revealed that L. reuteri is capable of producing ergothioneine. Although the known anti-inflammatory and anti-oxidative actions of ergothioneine suggested that the increased fecal ergothioneine levels may be related to intestinal anti-inflammatory defense mechanisms, no change was observed in the plasma ergothioneine levels during the same observation period, indicating that the defense mechanisms may not be sufficiently reflected in the body. As ergothioneine is a natural ingredient that is absorbed mainly from the upper gastrointestinal tract, we hypothesized that oral ergothioneine may exert antidepressant effects. As expected, oral administration of ergothioneine prior to and during the SDS paradigm had a preventative effect on SDS-induced depressive behaviors, such as social avoidance and depression-like sleep abnormalities, particularly those of rapid eye movement sleep. These findings indicate that ergothioneine, a metabolite of L. reuteri, may be a common substance in the microbiota-gut-brain axis that prevents stress-induced sleep disturbances, especially those associated with depression.
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Sleep Apnea Morbidity: A Consequence of Microbial-Immune Cross-Talk?
OSA has emerged as a highly prevalent public health problem that imposes important mid- and long-term consequences, namely cardiovascular, metabolic, cognitive, and cancer-related alterations. OSA is characterized by increased upper airway resistance, alveolar hypoventilation, and recurrent upper airway obstruction during sleep. Recurrent collapse of the upper airway develops with sleep onset and is associated with both intermittent hypoxemia and sleep fragmentation. The microbiome is a vast and complex polymicrobial ecosystem that coexists with the human organism, and it has been identified as playing significant roles in the development of host immunologic phenotypes. In humans and animal models, changes in gut microbial communities occur with lifestyle behaviors, such as smoking, long-distance travel, dietary preferences, physical exercise, and circadian rhythm disturbances. In parallel, diseases previously attributed in part to lifestyle such as obesity, coronary heart disease, depression, and asthma (also associated with OSA) are now claimed as microbiota related. We therefore posit that altered patterns of sleep and oxygenation, as seen in OSA, will promote specific alterations in gut microbiota that in turn will elicit the immunologic alterations that lead to OSA-induced end-organ morbidities. The present article assesses the potential mechanistic links between OSA-induced changes in gut microbiota and its morbid phenotypes.
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Gut microbiota, immunity and pain.
The interplay between microbiota and nervous system has been associated with a variety of diseases, including stress, anxiety, depression and cognition. The growing body of evidences on the essential role of gut microbiota in modulating acute and chronic pain has opened a new frontier for pain management. Gut microbiota is involved in the development of visceral, inflammatory and neuropathic pain. Bacterial alterations due to chronic opioid administration have been directly related to the development of drug tolerance, which can be potentially restored by the use of probiotics and antibiotics. In this review we describe the mechanisms underlying the brain/gut axis and the relationship between gut microbiota, immunity and pain.