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A global atlas of the gut virome reveals subtype-specific and functional alterations in irritable bowel syndrome.
The gut virome is a critical component of the microbiome-gut-brain axis; however, its role in irritable bowel syndrome (IBS) remains poorly understood due to limited sample sizes and geographic bias. We aimed to construct a comprehensive global atlas of the IBS gut virome to elucidate its composition, functional potential, and clinical relevance across diverse populations and IBS subtypes. We integrated multi-cohort data comprising 1,104 samples (790 IBS patients and 314 healthy controls) from 11 cohorts across 10 geographic regions. A standardized bioinformatic pipeline was employed to perform viral mining from metagenomic and virus-like particle-enriched metaviromic data. The IBS virome exhibited significant taxonomic alterations, with specific viral signatures distinguishing IBS-D, IBS-C, and IBS-M subtypes. Geographic region was identified as a significant factor influencing the viral community structure. Functionally, the IBS virome was enriched in auxiliary metabolic genes involved in carbon metabolism and neurotransmitter precursor synthesis (histidine and tryptophan metabolism), as well as a distinct profile of virulence factors and antibiotic resistance genes. Furthermore, in a specific cohort, certain viral taxa were significantly correlated with the severity of anxiety and depression. Machine learning models based on viral signatures achieved robust performance for IBS subtyping (area under the curve = 0.92). This study establishes a global baseline for the IBS gut virome, demonstrating that viral communities are dynamically shaped by geography and disease subtypes while encoding gene repertoires with the potential to influence host physiology, thereby providing a foundational resource for precision medicine.IMPORTANCEResearch on the human gut microbiome in IBS has focused primarily on bacteria, leaving the viral component as a vast and poorly understood reservoir. By profiling over 1,000 human samples globally, this study characterizes the taxonomic and functional features of the IBS gut virome. We demonstrate that these viral communities vary across geographic populations and IBS subtypes and are enriched in specific auxiliary metabolic genes, virulence factors, and antibiotic resistance genes. In addition, certain viral profiles show significant correlations with patient psychological symptoms such as anxiety and depression. This study also evaluates the potential of virome-based diagnostic biomarkers. Consequently, our findings provide a valuable reference for future in-depth research into the specific roles and mechanistic contributions of the gut virome in the pathogenesis of IBS.
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Pubertal probiotics mitigate lipopolysaccharide-induced programming of the hypothalamic-pituitary-adrenal axis in male mice only.
Puberty is a period of rapid cortical and neuronal development. Stress exposure during puberty programs the hypothalamic-pituitary-adrenal (HPA) axis responsiveness to future stressors. However, programming can result in an enduring maladaptation of the HPA axis activity and can be associated with long-term anxiety- and depression-like behaviours. Probiotic treatment mitigates the effect of stress on mental health, suggesting that the gut microbiome may mediate the programming of the HPA axis. However, the mechanism underlying this effect remains elusive. Thus, we investigated the effect of probiotic exposure on lipopolysaccharide (LPS)-induced programming of the HPA axis and glucocorticoid receptor (GR) expression in the paraventricular (PVN), basolateral amygdala (BLA), piriform cortex (PIR), and medial prefrontal cortex (mPFC). Male and female mice were exposed to either probiotics or control skim milk and were treated with either saline or LPS during puberty. Prior to euthanasia in adulthood, mice were restrained for 30 min. The results showed that pubertal LPS treatment permanently decreased GR expression in the PVN in milk fed control males. However, pubertal probiotic treatment blocked the LPS-induced decrease in GR expression in males. Given that this effect is limited to males, further research is required to better understand sex differences in the interactions between the gut microbiome and the programming of the HPA axis during puberty. Nevertheless, our findings suggest that the gut microbiome influences the neurophysiology of the HPA axis and mediates its programming in pubertal males. The prevention of GR reduction in the male PVN and PIR using probiotics illustrates the complexity of the gut-brain communication and compels continued investigation.
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Intermittent Fasting, Dietary Modifications, and Exercise for the Control of Gestational Diabetes and Maternal Mood Dysregulation: A Review and a Case Report.
Gestational diabetes mellitus (GDM) is a common pregnancy-related condition afflicting 5-36% of pregnancies. It is associated with many morbid maternal and fetal outcomes. Mood dysregulations (MDs, e.g., depression, distress, and anxiety) are common among women with GDM, and they exacerbate its prognosis and hinder its treatment. Hence, in addition to early detection and proper management of GDM, treating the associated MDs is crucial. Maternal hyperglycemia and MDs result from a complex network of genetic, behavioral, and environmental factors. This review briefly explores mechanisms that underlie GDM and prenatal MDs. It also describes the effect of exercise, dietary modification, and intermittent fasting (IF) on metabolic and affective dysfunctions exemplified by a case report. In this patient, interventions such as IF considerably reduced maternal body weight, plasma glucose, and psychological distress without any adverse effects. Thus, IF is one measure that can control GDM and maternal MDs; however, more investigations are warranted.
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The gut microbiota, HPA axis, and brain in adolescent-onset depression: Probiotics as a novel treatment.
Stress-associated disruptions in the development of frontolimbic regions may play a critical role in the emergence of adolescent-onset depression. These regions are particularly sensitive to Hypothalamic-Pituitary-Adrenal (HPA) axis signaling. The HPA axis is hyperactive in adolescent depression, and interventions that attenuate such hyperactivity hold promise as potential treatments. The Microbiome-Gut-Brain (MGB) axis is an important pathway through which stress dysregulates HPA-axis activity and thus exerts deleterious effects on the adolescent brain. Probiotic agents, which alter the gut microbiota composition by introducing bacterial strains with beneficial physiological effects, normalize aberrant HPA-axis activity and reduce depressive symptoms in both animal studies and adult clinical trials. While the potential utility of such agents in treating or preventing adolescent depression remains largely unexplored, recent data suggest the existence of an adolescent sensitive window during which probiotics may be especially efficacious in reducing depressive symptoms compared to effects observed in adult populations. In this review, we outline evidence that probiotic use may attenuate stress effects on frontolimbic development, providing a novel means of improving depressive symptoms among adolescent populations.
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A Randomised, Double-Blind, Placebo-Controlled Trial of Probiotic and Postbiotic Strains in Healthy Adults with Self-Reported Anxiety: Effects on Mood, Vitality, Quality of Life and Perceived Stress.
Background: Subclinical psychological symptoms-such as low mood, perceived stress, and poor sleep-affect a large portion of the population and can impair quality of life despite remaining below clinical thresholds. The gut-brain axis has emerged as a promising target for interventions that support emotional and psychological resilience. Probiotics and postbiotics are gaining attention for their potential to modulate mood and stress via microbiome-related mechanisms, but human evidence remains limited, particularly in non-clinical populations. Objectives: We aimed to assess the effects of a two-strain combination of live microorganisms alongside a two-strain combination of heat-treated inactivated microorganisms on outcomes associated with anxiety, mood, perceived stress, and quality of life in healthy adults experiencing mild stress. Methods: This study was conducted in two parts. In Part I, a randomized, double-blind, placebo-controlled study, 100 participants were randomized to receive either a blend of live microorganisms (Bifidobacterium longum CECT 7347 and Lactobacillus rhamnosus CECT 8361) or an identical placebo once daily for 12 weeks. In Part II, a pilot feasibility study, a subset of eight placebo non-responders from Part I received the heat-inactivated preparation of the same bacterial strains in a 6-week trial extension phase. For Parts I and II, the primary outcome was the change in the Hamilton Anxiety Rating Scale (HAM-A). Secondary outcomes included measures of mood (Beck Depression Inventory (BDI); Patient Health Questionnaire-9 (PHQ-9)), stress (state and trait anxiety inventory (STAI); Perceived Stress Scale (PSS)), sleep (Pittsburgh Sleep Quality Index (PSQI)), quality of life (36-item Short Form Survey (SF-36)), gastrointestinal symptoms (Gastrointestinal Symptom Rating Scale (GSRS)), salivary cortisol and microbiome modulation. Results: In Part I, there were no significant effects of the live blend on the HAM-A, indicating that the primary endpoint was not met. In addition, no significant effects were seen on the STAI or PSS scores when compared to the placebo. However, participants consuming the live blend trended toward a reduction in total PHQ-9 scores compared to placebo (p = 0.089), whilst preliminary exploratory analyses suggested an improvement in anhedonia (p = 0.045). Furthermore, there was a significant improvement in the vitality domain of the SF-36 compared to placebo (p = 0.017). On microbiome analysis, it was noted that consumption of the live blend was linked to the preservation of butyrate-producing bacteria, particularly members of the Pseudoflavonifractor genus and the Clostridium SGB6179 species. Furthermore, the abundance of B. longum species was found to be inversely associated with the total PSS Scores. In Part II, supplementation with the inactivated preparation resulted in significant within-group improvements for the vitality (p = 0.006) and social functioning (p = 0.010) domains of the SF-36 and improvements in PSS scores compared to baseline (p = 0.050). Conclusions: Supplementation with either the dual-strain live or inactivated formulations was associated with significant improvements in the vitality domain of the SF-36, whilst participants receiving the inactivated formulation demonstrated lower perceived stress and improved social functioning compared to baseline. Overall, the findings from this pilot study suggest that these two biotic consortia are well-tolerated and may be associated with improvements in measures of vitality in individuals with subclinical psychological symptoms. The subtle observations detected for stress and anhedonia suggest that further well-powered trials are needed to better characterize these findings, potentially in populations with greater baseline symptomatology.
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Chronic Visceral Pain: New Peripheral Mechanistic Insights and Resulting Treatments.
Chronic visceral pain is one of the most common reasons for patients with gastrointestinal disorders, such as inflammatory bowel disease or disorders of brain-gut interaction, to seek medical attention. It represents a substantial burden to patients and is associated with anxiety, depression, reductions in quality of life, and impaired social functioning, as well as increased direct and indirect health care costs to society. Unfortunately, the diagnosis and treatment of chronic visceral pain is difficult, in part because our understanding of the underlying pathophysiologic basis is incomplete. In this review, we highlight recent advances in peripheral pain signaling and specific physiologic and pathophysiologic preclinical mechanisms that result in the sensitization of peripheral pain pathways. We focus on preclinical mechanisms that have been translated into treatment approaches and summarize the current evidence base for directing treatment toward these mechanisms of chronic visceral pain derived from clinical trials. The effective management of chronic visceral pain remains of critical importance for the quality of life of suffers. A deeper understanding of peripheral pain mechanisms is necessary and may provide the basis for novel therapeutic interventions.
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Azithromycin preserves adult hippocampal neurogenesis and behavior in a mouse model of sepsis.
The mammalian hippocampus can generate new neurons throughout life. Known as adult hippocampal neurogenesis (AHN), this process participates in learning, memory, mood regulation, and forgetting. The continuous incorporation of new neurons enhances the plasticity of the hippocampus and contributes to the cognitive reserve in aged individuals. However, the integrity of AHN is targeted by numerous pathological conditions, including neurodegenerative diseases and sustained inflammation. In this regard, the latter causes cognitive decline, mood alterations, and multiple AHN impairments. In fact, the systemic administration of Lipopolysaccharide (LPS) from E. coli to mice (a model of sepsis) triggers depression-like behavior, impairs pattern separation, and decreases the survival, maturation, and synaptic integration of adult-born hippocampal dentate granule cells. Here we tested the capacity of the macrolide antibiotic azithromycin to neutralize the deleterious consequences of LPS administration in female C57BL6J mice. This antibiotic exerted potent neuroprotective effects. It reversed the increased immobility time during the Porsolt test, hippocampal secretion of pro-inflammatory cytokines, and AHN impairments. Moreover, azithromycin promoted the synaptic integration of adult-born neurons and functionally remodeled the gut microbiome. Therefore, our data point to azithromycin as a clinically relevant drug with the putative capacity to ameliorate the negative consequences of chronic inflammation by modulating AHN and hippocampal-related behaviors.
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Marked shifts in gut microbial structure and neurotransmitter metabolism in fresh inmates revealed a close link between gut microbiota and mental health: A case-controlled study.
BACKGROUND/OBJECTIVE: The gut microbiota plays a pivotal role in psychological health, but the mechanistic perspective between gut microbiome and mental health remains poorly understood. METHOD: The present case-controlled study recruited 30 unimprisoned subjects and 31 inmates that had been detained in jail for no more than a month. The mental health status, gut microbiota and blood NH3, H2S, 5-hydroxy trptamine and dopamine levels were measured. RESULTS: Compared with unimprisoned controls, the fresh inmates exhibited significantly higher scores on anxiety and depression. Both phylogenetic structure and functional genes of the gut microbiota markedly shifted in inmates. Inmates was more Bacteroides-dominated, while unimprisoned subjects were more Prevotella-dominated. Short-chain fatty acids (SCFAs)-producing genera were largely decreased in inmates and were negatively related to mental disorder scores, while Bacteroidetes and Proteobacteria were positive to anxiety and depression scores. Simultaneously, the inmates possessed reduced genes that participate in amino acids, carbohydrates and vitamin cofactors metabolism, but enriched genes that involved in the neurotransmitter-producing Shikimate pathway. Correlation analysis revealed that Anaerotruncus and Prevotella were negative to depression score, and Enterococcus was negative to anxiety score. CONCLUSIONS: Our results revealed potential link between gut microbiota and mental health, leading further support to the microbiota-gut-brain axis theory.
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Gut mycobiome and neuropsychiatric disorders: insights and therapeutic potential.
BACKGROUND: The human gut mycobiome, a minor but integral component of the gut microbiome, has emerged as a significant player in host homeostasis and disease development. While bacteria have traditionally been the focus of gut microbiome studies, recent evidence suggests that fungal communities (mycobiota) may also play a crucial role in modulating health, particularly in neuropsychiatric disorders. OBJECTIVE: This review aims to provide a comprehensive overview of current knowledge on the relationship between the gut mycobiome and neuropsychiatric disorders, exploring the potential of targeting fungal communities as a novel therapeutic strategy. METHODS: We summarized recent findings from metagenomic analyses that characterize the diversity and composition of gut mycobiota and discuss how these communities interact with the host and other microorganisms via the gut-brain axis. Key methodologies for studying mycobiota, such as high-throughout sequencing and bioinformatics approaches, were also reviewed to highlight advances in the field. RESULTS: Emerging research links gut mycobiota dysbiosis to conditions such as schizophrenia, Alzheimer's disease, autism spectrum disorders, bipolar disorder, and depression. Studies indicate that specific fungal populations, such as Candida and Saccharomyces, may influence neuroinflammation, gut permeability and immune responses, thereby affecting mental health outcomes. CONCLUSION: Understanding the gut mycobiome's role in neuropsychiatric disorders opens new avenues for therapeutic interventions, including antifungal treatments, probiotics, and dietary modifications. Future research should integrate multi-omics approaches to unravel the complex interkingdom interactions within the gut ecosystem, paving the way for personalized medicine in mental health care.
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Therapeutic Interventions of Gut-Brain Axis as Novel Strategies for Treatment of Alcohol Use Disorder Associated Cognitive and Mood Dysfunction.
Alcohol use disorders (AUD) is characterized by persistent or intermittent alcohol cravings and compulsive drinking. The functional changes in the central nervous system (CNS) after alcohol consumption are alcohol-associated cognitive impairment and mood disorders, which are major health issues reported in AUDs. Studies have shown that transferring the intestinal microbiota from AUDs patients to germ-free animals causes learning and memory dysfunction, depression and anxiety-like behavior, indicating the vital role of intestinal microbiota in development of neuropsychiatric disorders in AUD. Intestinal flora composition of AUD patients are significantly different from normal people, suggesting that intestinal flora imbalance orchestrate the development of neuropsychiatric disorders in AUD. Studies suggests that gut microbiome links bidirectional signaling network of the enteric nervous system (ENS) to central nervous system (CNS), forming gut-microbe-brain axis (brain-gut axis). In this review, we discussed pathogenesis and possible treatment of AUD-induced cognitive deficits, anxiety, and depression disorders. Further, we described the mechanism of intestinal flora imbalance and dysfunction of hippocampus-amygdala-frontal cortex (gut-limbic circuit system dysfunction). Therefore, we postulate therapeutic interventions of gut-brain axis as novel strategies for treatment of AUD-induced neuropsychiatric disorders.