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Virobiome-mediated regulation of microbiota-gut-brain axis signaling and neuroimmune homeostasis.
The human gut-brain axis (GBA) is increasingly recognized as a complex bidirectional communication system integrating microbial, neural, endocrine, and immune networks that shape neurological health. While bacterial contributions to this dialogue have been extensively characterized, the viral component of the gut ecosystem, the virome, has emerged as an important component associated with host physiological regulation. This review synthesizes evidence suggesting that bacteriophages and eukaryotic viruses may contribute to microbial and immune homeostasis and may influence signaling along the microbiota-gut-brain axis. In experimental studies, Bacteriophages have been shown to influence microbial community structure through lytic and lysogenic cycles, horizontal gene transfer, and metabolic modulation, indirectly regulating production of neuroactive metabolites such as short-chain fatty acids and tryptophan derivatives which in turn have been linked to blood brain barrier integrity and modulate microglial activation. In observational human studies and experimental models, eukaryotic viruses including Epstein Barr virus and cytomegalovirus have been associated with systemic inflammation, molecular mimicry, and cytokine dysregulation, amplifying neuroimmune cascades implicated in Alzheimer's disease (AD), multiple sclerosis (MS), autism spectrum disorder (ASD), and major depressive disorder (MDD). The convergence of viral-bacterial interactions highlights a transkingdom signaling network shaping neuroinflammatory tone and influencing disease susceptibility. Emerging experimental strategies, including precision phage therapy, engineered probiotics incorporating CRISPR-based antiviral systems, and fecal virome transplantation (FVT), are being explored as potential approaches to modulate virome-microbiome interactions. Integration of multiomics platforms with artificial intelligence-driven modeling will be critical for clarifying the temporal and mechanistic relationships between virome dynamics and neurological function. Collectively, these insights highlight the gut virobiome as a potentially important contributor to neuroimmune equilibrium and illuminate avenues for microbiome-informed diagnostics and interventions in neurodegenerative and neuropsychiatric disorders. This review therefore highlights the often underappreciated role of the gut virobiome and proposes an integrative conceptual model linking virome dynamics with microbiota-gut-brain axis signaling.
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Tryptophan Metabolism and Gut-Brain Homeostasis.
Tryptophan is an essential amino acid critical for protein synthesis in humans that has emerged as a key player in the microbiota-gut-brain axis. It is the only precursor for the neurotransmitter serotonin, which is vital for the processing of emotional regulation, hunger, sleep, and pain, as well as colonic motility and secretory activity in the gut. Tryptophan catabolites from the kynurenine degradation pathway also modulate neural activity and are active in the systemic inflammatory cascade. Additionally, tryptophan and its metabolites support the development of the central and enteric nervous systems. Accordingly, dysregulation of tryptophan metabolites plays a central role in the pathogenesis of many neurologic and psychiatric disorders. Gut microbes influence tryptophan metabolism directly and indirectly, with corresponding changes in behavior and cognition. The gut microbiome has thus garnered much attention as a therapeutic target for both neurologic and psychiatric disorders where tryptophan and its metabolites play a prominent role. In this review, we will touch upon some of these features and their involvement in health and disease.
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Investigating the causal relationship of gut microbiota with GERD and BE: a bidirectional mendelian randomization.
BACKGROUND: Gut microbiota(GM) have been proven associated with lots of gastrointestinal diseases, but its causal relationship with Gastroesophageal reflux disease(GERD) and Barrett's esophagus(BE) hasn't been explored. We aimed to uncover the causal relation between GM and GERD/BE and potential mediators by utilizing Mendelian Randomization(MR) analysis. METHODS: Summary statistics of GM(comprising 301 bacteria taxa and 205 metabolism pathways) were extracted from MiBioGen Consortium(N = 18,340) and Dutch Microbiome Project(N = 7,738), GERD and BE from a multitrait meta-analysis(NGERD=602,604, NBE=56,429). Bidirectional two-sample MR analysis and linkage disequilibrium score regression(LDSC) were used to explore the genetic correlation between GM and GERD/BE. Mediation MR analysis was performed for the risk factors of GERD/BE, including Body mass index(BMI), weight, type 2 diabetes, major depressive disorder(MDD), smoking initiation, alcohol consumption, and dietary intake(including carbohydrate, sugar, fat, protein intake), to detect the potential mediators between GM and GERD/BE. RESULTS: 11 bacterial taxa and 13 metabolism pathways were found associated with GERD, and 18 taxa and 5 pathways exhibited causal relationship with BE. Mediation MR analysis suggested weight and BMI played a crucial role in these relationships. LDSC identified 1 taxon and 4 metabolism pathways related to GERD, and 1 taxon related to BE. Specie Faecalibacterium prausnitzii had a suggestive impact on both GERD(OR = 1.087, 95%CI = 1.01-1.17) and BE(OR = 1.388, 95%CI = 1.03-1.86) and LDSC had determined their correlation. Reverse MR indicated that BE impacted 10 taxa and 4 pathways. CONCLUSIONS: This study established a causal link between gut microbiota and GERD/BE, and identified the probable mediators. It offers new insights into the role of gut microbiota in the development and progression of GERD and BE in the host.
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The Gut Microbiome in Amyotrophic Lateral Sclerosis: Emerging Mechanisms and Therapeutic Potential.
Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder marked by progressive loss of motor neurons and a median survival of 2 to 3 years after symptom onset. Despite advances in genetics, particularly the identification of mutations in C9ORF72, SOD1, and TDP 43, substantial variability in disease onset and progression remains unexplained. Mounting evidence points to the gut microbiome as a potential modifier of ALS biology. Microbial communities within the intestine influence systemic and central immune responses, energy metabolism, and the bioavailability of nutrients and therapeutic agents. Animal studies reveal that dysbiosis contributes to intestinal barrier dysfunction, immune activation, and altered metabolite production, while supplementation with beneficial metabolites such as butyrate or nicotinamide can delay disease progression and extend survival. Human studies, though inconsistent in their findings, consistently identify microbial imbalances and loss of diversity in subsets of patients. The gut-brain axis provides a plausible framework for these effects, as microbial products can signal through endocrine, neural, and immune pathways to influence central nervous system function. Beyond motor decline, microbiota alterations may also contribute to non-motor symptoms such as depression, anxiety, and gastrointestinal dysfunction, further shaping quality of life. While methodological variability complicates interpretation, integration of microbiome research with host genomics and metabolomics offers a path toward precision medicine. Targeting microbial composition and function may ultimately represent a novel therapeutic approach capable of modifying both disease biology and patient outcomes in ALS.
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The gut microbiome and neuropsychiatric disorders: implications for attention deficit hyperactivity disorder (ADHD).
Neuropsychiatric disorders (NPDs) such as depression, anxiety, bipolar disorder, autism spectrum disorder (ASD) and attention deficit hyperactivity disorder (ADHD) all relate to behavioural, cognitive and emotional disturbances that are ultimately rooted in disordered brain function. More specifically, these disorders are linked to various neuromodulators (i.e. serotonin and dopamine), as well as dysfunction in both cognitive and socio-affective brain networks. Increasing evidence suggests that the gut environment, and particularly the microbiome, plays a significant role in individual mental health. Although the presence of a gut-brain communication axis has long been established, recent studies argue that the development and regulation of this axis is dictated by the gut microbiome. Many studies involving both animals and humans have connected the gut microbiome with depression, anxiety and ASD. Microbiome-centred treatments for individuals with these same NPDs have yielded promising results. Despite its recent rise and underlying similarities to other NPDs, both biochemically and symptomatically, connections between the gut microbiome and ADHD currently lag behind those for other NPDs. We demonstrate that all evidence points to the importance of, and dire need for, a comprehensive and in-depth analysis of the role of the gut microbiome in ADHD, to deepen our understanding of a condition that affects millions of individuals worldwide.
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Gastrointestinal symptoms, gut microbiome, probiotics and prebiotics in anorexia nervosa: A review of mechanistic rationale and clinical evidence.
Recent research has revealed the pivotal role that the gut microbiota might play in psychiatric disorders. In anorexia nervosa (AN), the gut microbiota may be involved in pathophysiology as well as in the gastrointestinal (GI) symptoms commonly experienced. This review collates evidence for the potential role of gut microbiota in AN, including modulation of the immune system, the gut-brain axis and GI function. We examined studies comparing gut microbiota in AN with healthy controls as well as those looking at modifications in gut microbiota with nutritional treatment. Changes in energy intake and nutritional composition influence gut microbiota and may play a role in the evolution of the gut microbial picture in AN. Additionally, some evidence indicates that pre-morbid gut microbiota may influence risk of developing AN. There appear to be similarities in gut microbial composition, mechanisms of interaction and GI symptoms experienced in AN and other GI disorders such as inflammatory bowel disease and functional GI disorders. Probiotics and prebiotics have been studied in these disorders showing therapeutic effects of probiotics in some cases. Additionally, some evidence exists for the therapeutic benefits of probiotics in depression and anxiety, commonly seen as co-morbidities in AN. Moreover, preliminary evidence for the use of probiotics in AN has shown positive effects on immune modulation. Based on these findings, we discuss the potential therapeutic role for probiotics in ameliorating symptoms in AN.
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Integrative Therapies in Anxiety Treatment with Special Emphasis on the Gut Microbiome.
Over the past decade, research has shown that diet and gut health affects symptoms expressed in stress related disorders, depression, and anxiety through changes in the gut microbiota. Psycho-behavioral function and somatic health interaction have often been ignored in health care with resulting deficits in treatment quality and outcomes. While mental health care requires the professional training in counseling, psychotherapy and psychiatry, complimentary therapeutic strategies, such as attention to a nutritional and diverse diet and supplementation of probiotic foods, may be integrated alongside psychotherapy treatment models. Development of these alternative strategies is predicated on experimental evidence and diligent research on the biology of stress, fear, anxiety-related behaviors, and the gut-brain connection. This article provides a brief overview on biological markers of anxiety and the expanding nutritional literature relating to brain health and mental disorders. A case study demonstrates an example of a biopsychosocial approach integrating cognitive psychotherapy, dietary changes, and mindfulness activities, in treating symptoms of anxiety. This case study shows a possible treatment protocol to explore the efficacy of targeting the gut-brain-axis that may be used as an impetus for future controlled studies.
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Microbiome and metabolome integrally reveal the anti-depression effects of Cistanche deserticola polysaccharides from the perspective of gut homeostasis.
Polysaccharides are one of the active components of Cistanche deserticola (CD). Cistanche deserticola polysaccharides (CDPs) significantly regulate gut microbiota, immune activity, and neuroprotective functions. However, it merely scratches the surface that the anti-depression effects of CDPs. We aimed to demonstrate the anti-depression effects of CDPs and the underlying mechanisms from the perspectives of gut homeostasis by behavioral evaluations and applying integrally microbiome, metabolome, and molecular biology. CDPs showed significant effects on improving abnormal behaviors of depressed rats. Additionally, CDPs maintained Th17/Treg balance and modulated gut immunity of depressed rats. Comprehensive microbiome and metabolome analysis showed that CDPs significantly ameliorated abundances of beneficial bacteria, and increased the contents of SCFAs, consequently maintaining gut homeostasis. Besides, the anti-depression effects of CDPs involved in amino acid metabolism including BCAAs, glutamine, etc., maintaining metabolic balance. The current findings provide not only deep understanding of depression focusing on gut, but also evidence about the anti-depression effects of CDPs, broadening clinic applications of CDPs. Of note, the present study is of significance in a long run, in terms of providing novel strategies and protocols for revealing mechanisms of anti-depression drugs, and for the discovery of new antidepressants and functional foods from natural products.
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Effect of oral tryptamines on the gut microbiome of rats-a preliminary study.
BACKGROUND: Psilocybin and related tryptamines have come into the spotlight in recent years as potential therapeutics for depression. Research on the mechanisms of these effects has historically focused on the direct effects of these drugs on neural processes. However, in addition to such neural effects, alterations in peripheral physiology may also contribute to their therapeutic effects. In particular, substantial support exists for a gut microbiome-mediated pathway for the antidepressant efficacy of other drug classes, but no prior studies have determined the effects of tryptamines on microbiota. METHODS: To address this gap, in this preliminary study, male Long Evans rats were treated with varying dosages of oral psilocybin (0.2 or 2 mg/kg), norbaeocystin (0.25 or 2.52 mg/kg), or vehicle and their fecal samples were collected 1 week and 3 weeks after exposure for microbiome analysis using integrated 16S ribosomal DNA sequencing to determine gut microbiome composition. RESULTS: We found that although treatment with neither psilocybin nor norbaeocystin significantly affected overall microbiome diversity, it did cause significant dose- and time-dependent changes in bacterial abundance at the phylum level, including increases in Verrucomicrobia and Actinobacteria, and decreases in Proteobacteria. CONCLUSION AND IMPLICATIONS: These preliminary findings support the idea that psilocybin and other tryptamines may act on the gut microbiome in a dose- and time-dependent manner, potentially identifying a novel peripheral mechanism for their antidepressant activity. The results from this preliminary study also suggest that norbaeocystin may warrant further investigation as a potential antidepressant, given the similarity of its effects to psilocybin.
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Identifying psychiatric disorder-associated gut microbiota using microbiota-related gene set enrichment analysis.
Psychiatric disorders are a group of complex psychological syndromes with high prevalence. It has been reported that gut microbiota has a dominant influence on the risks of psychiatric disorders through gut microbiota-brain axis. We extended the classic gene set enrichment analysis (GSEA) approach to detect the association between gut microbiota and complex diseases using published genome-wide association study (GWAS) and GWAS of gut microbiota summary data. We applied our approach to real GWAS data sets of five psychiatric disorders, including attention deficiency/hyperactive disorder (ADHD), autism spectrum disorder (AUT), bipolar disorder (BD), schizophrenia (SCZ) and major depressive disorder (MDD). To evaluate the performance of our approach, we also tested the genetic correlations of obesity and type 2 diabetes with gut microbiota. We identified several significant associations between psychiatric disorders and gut microbiota, such as ADHD and genus Desulfovibrio (P = 0.031), order Clostridiales (P = 0.034). For AUT, association signals were observed for genera Bacteroides (P = 0.012) and Desulfovibrio (P = 0.033). Genus Desulfovibrio (P = 0.005) appeared to be associated with BD. For MDD, association signals were observed for genus Desulfovibrio (P = 0.003), order Clostridiales (P = 0.004), family Lachnospiraceae (P = 0.007) and genus Bacteroides (P = 0.007). Genus Desulfovibrio (P = 0.012) and genus Bacteroides (P = 0.038) appeared to be associated with SCZ. Our study results provide novel clues for revealing the roles of gut microbiota in psychiatric disorders. This study also illustrated the good performance of GSEA approach for exploring the relationships between gut microbiota and complex diseases.