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Antidepressants fluoxetine and amitriptyline induce alterations in intestinal microbiota and gut microbiome function in rats exposed to chronic unpredictable mild stress.
Antidepressant medications are known to modulate the central nervous system, and gut microbiota can play a role in depression via microbiota-gut-brain axis. But the impact of antidepressants on gut microbiota function and composition remains poorly understood. Thus this study assessed the effect of serotonin reuptake inhibitor antidepressant fluoxetine (Flu) and tricyclic antidepressant amitriptyline (Ami) administration on gut microbiota composition, diversity, and species abundance, along with microbial function in a chronic unpredictable mild stress (CUMS)-induced depression rat model. Oral administration of Ami and Flu significantly altered the overall gut microbiota profile of CUMS-induced rats, as assessed using the permutational multivariate analysis of variance test. At the phylum level, 6-week of antidepressant treatment led to a decreased Firmicutes/Bacteroidetes ratio due to an enhanced Bacteroidetes and reduced Firmicutes relative abundance. Flu was more potent than Ami at altering the Firmicutes and Bacteroidetes levels in the CUMS rats. At the family level, both antidepressants significantly increased the abundance of Porphyromonadaceae. However, an increased Bacteroidaceae level was significantly associated with Ami, not Flu treatment. Furthermore, at the genus level, an increase in the relative abundance of Parabacteroides, Butyricimonas, and Alistipes was observed following Ami and Flu treatment. Subsequent metagenomics and bioinformatics analysis further indicated that Ami and Flu likely also modulated metabolic pathways, such as those involved in carbohydrate metabolism, membrane transport, and signal transduction. Additionally, both antidepressants affected antibiotic resistome, such as for aminoglycoside (aph3iiiA), multidrug (mdtK, mdtP, mdtH, mdtG, acrA), and tetracycline (tetM) resistance in CUMS rats. These data clearly illustrated the direct impact of oral administration of Flu and Ami on the gut microbiome, thus set up the foundation to reveal more insights on the therapeutic function of the antidepressants and their overall contribution to host health.
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Efficacy of Lactobacillus spp. Interventions to Modulate Mood Symptoms: A Scoping Review of Clinical Trials.
Probiotics containing Lactobacillus spp. have demonstrated immunological and gastrointestinal benefits and may aid in recovery from mood disorders. However, evidence of their mood-modulating efficacy remains inconsistent. Aim: To analyze the efficacy of probiotic interventions with Lactobacillus spp. in modulating mood in humans. A scoping review was conducted following the PRISMA guidelines. A systematic search of the PubMed and Scopus databases was performed using nine Boolean combinations of the terms "mental", "mental diseases", "mental disorders", "gastrointestinal microbiome", "gut microbiome", "gut microbiota", and "lactobacillus". The search was limited to clinical trials published in English and limited to ten years of publication. Eligible studies met the following criteria: (a) probiotic interventions in adults, with or without mood disturbances; (b) the use of Lactobacillus spp., either alone or in combination; (c) mood assessment instruments applied pre- and post-intervention; and (d) reporting of probiotic concentrations. Trials involving populations with other psychiatric or neurological diagnoses or those combining probiotics with additional mood-modulating nutrients were excluded. From 3291 records, 17 clinical trials met the inclusion criteria. Data extracted included the author, year, population, country of origin, probiotic strain(s), dosage, intervention mode and duration, and outcomes related to the microbial composition, biomarkers, and microbial metabolites. Trials were categorized by probiotic type (single vs. multi-species) and participant profile (healthy individuals and those with depressive symptoms or specific physiological conditions). Preliminary evidence from single-strain interventions, particularly high-dose L. plantarum administered for ≥8 weeks, suggests potential improvements in anxiety, sleep quality, and inflammatory biomarkers. Multi-species formulations yielded reductions in depressive symptoms and changes in neurobiological markers. Nonetheless, substantial heterogeneity in strains, dosages, durations, and outcome measures limited cross-study comparisons. Lactobacillus spp. interventions show promising mood-modulating potential, especially with specific strains and prolonged administration. Standardized protocols, rigorous controls, and clearly defined clinical cohorts are needed to establish robust, evidence-based recommendations.
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Consequences of Western and Mediterranean Diets' Nutrients on the Microbiota-Gut-Brain Axis.
Background: The prevalence of neurodegenerative diseases like Alzheimer's and mental disorders like depression or anxiety appears higher in patients with gastrointestinal tract diseases like inflammatory bowel disease (IBD). Conversely, depressed patients have higher rates of gastrointestinal disorders. These observations suggest bidirectional communication between the brain and the gastrointestinal tract, the so-called "gut-brain axis". Moreover, an altered microbiota, called "dysbiosis", has been reported in these diseases, highlighting the network between gut microbes and their host. The emergence of the microbiota as a key regulator of the gut-brain dialog has led to the establishment of the concept of the "microbiota-gut-brain axis". Objectives: In this narrative review, we outline the main interaction channels between the gastrointestinal tract and the brain. Then, we summarize current knowledge of two major diets (i.e., Western and Mediterranean diets) and the principal dietary components that modulate the microbiota-gut-brain axis to discuss the mechanisms putatively involved in intestinal, psychiatric, and neurological disorders. Conclusions: Diet is a major factor influencing the gut microbiota, and consequently, also putatively systemic mechanisms through the microbiota-gut-brain axis. Indeed, the composition of the diet is crucial for health and disease. Despite the main role of diet, the physiological, cellular, or molecular mechanisms involved in the complex communication between the microbiome, gut, and brain are still poorly understood.
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A preliminary study of gut microbiome variation and HPA axis reactivity in healthy infants.
The Hypothalamic Pituitary Adrenal (HPA) axis regulates hormonal responses to stress in both humans and animals and is dysregulated in a wide range of psychiatric disorders. There is strong evidence from rodent studies that gut microbial composition influences HPA axis development. In humans, variation in the gut microbiome has been associated with several psychological domains including depression and cognitive development, but studies focused on HPA axis development are still lacking. We tested whether differences in microbial composition are associated with HPA axis reactivity in a pilot study of 34 healthy human infants. HPA axis reactivity was assessed by measuring salivary cortisol in samples taken both before and after a heel stick, and 16S rRNA amplicon sequencing was used for identification and relative quantification of bacterial taxa. Subjects' alpha diversity levels showed a moderate positive association with their cortisol reactivity at one month of age. Exploratory genus-level analyses suggest that Staphylococcus, Prevotella, and genera in the order Lachnospiraceae may be related to cortisol reactivity at one month as well. The current study gives support for the endocrine pathway as a potential mediator in the microbiome-gut-brain axis during infancy, and as such provides motivation for future clinical work to support the development of stress-response systems through the manipulation of gut microbes.
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Harnessing Gut Microbes for Mental Health: Getting From Here to There.
There has been an explosion of interest in the study of microorganisms inhabiting the gastrointestinal tract (gut microbiota) and their impact on host health and physiology. Accumulating data suggest that altered communication between gut microbiota and host systems could participate in disorders such as obesity, diabetes mellitus, and autoimmune disorders as well as neuropsychiatric disorders, including autism, anxiety, and major depressive disorders. The conceptual development of the microbiome-gut-brain axis has facilitated understanding of the complex and bidirectional networks between gastrointestinal microbiota and their host, highlighting potential mechanisms through which this environment influences central nervous system physiology. Communication pathways between gut microbiota and the central nervous system could include autonomic, neuroendocrine, enteric, and immune systems, with pathology resulting in disruption to neurotransmitter balance, increases in chronic inflammation, or exacerbated hypothalamic-pituitary-adrenal axis activity. However, uncertainty remains regarding the generalizability of controlled animal studies to the more multifaceted pattern of human pathophysiology, especially with regard to the therapeutic potential for neuropsychiatric health. This narrative review summarizes current understanding of gut microbial influence over physiological function, with an emphasis on neurobehavioral and neurological impairment based on growing understanding of the gut-brain axis. Experimental and clinical data regarding means of therapeutic manipulation of gut microbiota as a novel treatment option for mental health are described, and important knowledge gaps are identified and discussed.
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Arketamine for cognitive impairment in psychiatric disorders.
Cognitive impairment has been observed in patients with various psychiatric disorders, including schizophrenia, major depressive disorder (MDD), and bipolar disorder (BD). Although modern therapeutic drugs can improve certain symptoms (i.e., psychosis, depression) in these patients, these drugs have not been found to improve cognitive impairment. The N-methyl-D-aspartate receptor antagonist (R,S)-ketamine has attracted attention as a rapidly acting antidepressant. In addition to its robust antidepressant effects, (R,S)-ketamine has been suggested to improve cognitive impairment in patients with MDD and BD, despite causing cognitive impairment in healthy control subjects. (R,S)-ketamine is a racemic mixture of equal amounts of (R)-ketamine (or arketamine) and (S)-ketamine (or esketamine). Arketamine has been found to have more potent antidepressant-like actions than esketamine in rodents. Interestingly, arketamine, but not esketamine, has been suggested to improve phencyclidine-induced cognitive deficits in mice. Furthermore, arketamine has been suggested to ameliorate cognitive deficits in rodent offspring after maternal immune activation. In the current article, it is proposed that arketamine has therapeutic potential for treating cognitive impairment in patients with psychiatric disorders. Additionally, the potential role of the gut-microbiome-brain axis in cognitive impairment in psychiatric disorders is discussed.
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Microbiota-gut-brain axis in health and disease: Is NLRP3 inflammasome at the crossroads of microbiota-gut-brain communications?
Growing evidence highlights the relevance of microbiota-gut-brain axis in the maintenance of brain homeostasis as well as in the pathophysiology of major neurological and psychiatric disorders, including Parkinson's disease (PD), Alzheimer's disease (AD), multiple sclerosis (MS), autism spectrum disorder (ASD) and major depressive disorder (MDD). In particular, changes in gut microbiota can promote enteric and peripheral neurogenic/inflammatory responses, which, in turn, could contribute to neuroinflammation and neurodegeneration in the central nervous system (CNS). Of note, the nucleotide-binding oligomerization domain leucine rich repeat and pyrin domain-containing protein 3 (NLRP3) inflammasome acts as a key player in both coordinating the host physiology and shaping the peripheral and central immune/inflammatory responses in CNS diseases. In this context, there is pioneering evidence supporting the existence of a microbiota-gut-inflammasome-brain axis, in which enteric bacteria modulate, via NLRP3 signaling, inflammatory pathways that, in turn, contribute to influence brain homeostasis. The present review provides an overview of current knowledge on the role of microbiota-gut-inflammasome-brain axis in the major CNS diseases, including PD, AD, MS, ASD and MDD. In particular, though no direct and causal correlation among altered gut microbiota, NLRP3 activation and brain pathology has been demonstrated and in-depth studies are needed in this setting, our purpose was to pave the way to a novel and pioneering perspective on the pathophysiology of CNS disorders. Our intent was also to highlight and discuss whether alterations of microbiota-gut-inflammasome-brain axis support a holistic view of the pathophysiology of CNS diseases, even though each disorder displays a different clinical picture.
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Maternal gut microbiota in the postpartum Period: A Systematic review.
Studies have demonstrated the importance of the gut microbiota during pregnancy, and there is emerging literature on the postpartum maternal gut microbiota. The primary objective of this paper was to synthesize the literature on the postpartum gut microbiome composition and diversity measured in stool samples from healthy mothers of predominantly term infants. The secondary objectives were (1) to identify biological and environmental factors that influence postpartum maternal gut microbiota and (2) to assess health conditions and clinical intermediate measures associated with postpartum gut microbiota changes in all mothers. Electronic searches were conducted November 9, 2020 and updated July 25, 2021 without publication time limits on PubMed, Embase, CINHAL, Scopus, Cochrane Library, BioArchives, and OpenGrey.eu. Primary research on maternal gut microbiota in the postpartum (up to one year after childbirth) were eligible. Postpartum gut microbiota comparisons to pregnancy or non-pregnancy gut microbiota were of interest, therefore, studies examining these in addition to the postpartum were included. Studies were excluded if they were only conducted in animals, infants, pregnancy, or microbiome of other body locations (e.g., vaginal). Data extraction of microbial composition and diversity were completed and synthesized narratively. Studies were assessed for risk of bias. A total of 2512 articles were screened after deduplication and 27 were included in this review. Of the 27 included studies, 22 addressed the primary objective. Firmicutes was the predominant phylum in the early (<6 weeks) and late postpartum (6 weeks to 1 year). In early postpartum, Bacteroides was the predominant genus. Findings from longitudinal assessments of alpha and beta diversity from the early to the late postpartum varied. Nineteen of the 27 studies assessed biological and environmental factors influencing the postpartum gut microbial profile changes. Timing of delivery, probiotic supplementation, triclosan exposure, and certain diets influenced the postpartum gut microbiota. Regarding health conditions and intermediate clinical measures assessed in 8 studies; inflammatory bowel disease, postpartum depression, early-onset preeclampsia, gestational diabetes, excessive gestational weight gain, and anthropometric measures such as body mass index and waist-to-hip ratio were related to gut microbiota changes. There is limited data on the maternal postpartum gut microbiota and how it influences maternal health. We need to understand the postpartum maternal gut microbiome, establish how it differs from non-pregnancy and pregnancy states, and determine biological and environmental influencers. Future research of the gut microbiome's significance for the birthing parent in the postpartum could lead to a new understanding of how to improve maternal short and long-term health.
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Simulated shift work schedules disrupts circadian rhythms and behavior in mice.
Shift work has become a major cause of circadian rhythm disruption in modern society. This study investigated the systemic consequences of shift schedules by subjecting mice to different light-dark (LD) cycles: non-24-h cycles (rapidly rotating groups A and B) and 24-h cycles (group C and control group). We performed behavioral tests, serum hormone measurements, transcriptomic analysis of suprachiasmatic nucleus (SCN) genes, and gut microbiome analysis. The results showed that the mice exhibited significant body weight gain after altering LD cycle compared with the control group. In groups exposed to non-24-h cycles, the circadian expression rhythms of core clock genes (Per, Cry, and Bmal1) in the SCN were lost. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses revealed that genes in the SCN losing rhythmicity were significantly enriched in metabolic and regulatory pathways, disrupting endocrine and metabolic rhythms and ultimately compromising health. The circadian rhythms of key hormones like melatonin and dopamine were also lost. Concurrently, these central disruptions drove peripheral pathology, including gut microbiota dysbiosis (altered Firmicutes/Bacteroidota ratio, reduced Verrucomicrobia) and a profound loss of gut microbial diurnal oscillations. Behaviorally, this multisystem discord manifested as significantly increased anxiety-like and depression-like behaviors and fatigue (P < 0.05), whereas spatial memory remained intact, indicating selective affective vulnerability. SCN collapse, together with hormonal chaos, desynchronizes the gut microbiome, potentially promoting inflammation and metabolic dysfunction that further disrupts central regulation. These findings provide a physiological foundation for understanding the health consequences of circadian disruption and may help guide the future design of healthier shift work schedules.NEW & NOTEWORTHY Systematic comparison of multiple simulated shift schedules in mice reveals that non-24-h light-dark cycles, but not fixed 24-h shifted cycles, abolish suprachiasmatic nucleus core clock gene (Per, Cry, Bmal1) rhythms, disrupt melatonin and dopamine, and desynchronize gut microbiota at the phylum level. These central and peripheral disruptions selectively exacerbate anxiety- and depression-like behaviors without impairing spatial memory, revealing a hierarchical disintegration of circadian organization. The findings provide a physiological framework for evidence-based shift scheduling.
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Musculoskeletal microbiology: The utility of the microbiome in orthopedics.
The past 15 years have witnessed a renaissance in the study of the microbes that colonize the human body. The vast majority of the human microbiome resides within the gut. Alterations to the gut microbiome have been associated with the pathogenesis and progression of wide-ranging diseases throughout the body-including atherosclerosis, depression, and obesity. Our understanding of the effects of the gut microbiome on the musculoskeletal system remains in its infancy, but preclinical work has demonstrated an effect of the gut microbiome on the success of orthopedic surgical procedures, osteoporosis, osteoarthritis, and muscle mass. In this perspective I review preclinical findings demonstrating that an impaired presurgical gut microbiome can increase the likelihood of developing periprosthetic joint infection and how alterations in the gut microbiome can reduce bone strength by impairing bone tissue material properties. In addition to discussing these examples, I review the hypothesis that many chronic non-communicable diseases have become more prevalent in modern industrialized societies as a result of changes in the composition of the gut microbiome resulting from changes in environment/lifestyle (diet, sanitation, antibiotic use). The most burdensome musculoskeletal disorders are chronic and non-communicable and may therefore be related to generational shifts in the composition of the gut microbiome, a possibility I illustrate by reviewing changes in the prevalence of osteoarthritis over the last century. Microbiome-based therapeutics are potentially innocuous, inexpensive, and have the potential to be effective with only occasional use, making them attractive for addressing the needs of chronic and/or slowly progressing musculoskeletal disorders.