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Gut-brain axis in post-traumatic stress disorder: microbial - mediated mechanisms and new therapeutic approaches - A narrative review.
Post-traumatic stress disorder (PTSD) is a severe mental disorder that occurs after experiencing or witnessing a traumatic event. Not only does this disorder severely impair the quality of life and emotional wellbeing of patients, but in recent years the global rate of PTSD diagnoses has increased to 1.5-2 times, and the prevalence of PTSD associated with COVID-19 events in particular has surged to 10%-25%, underscoring the urgency of developing effective treatments. The lifetime prevalence of PTSD in the general population is estimated to be approximately 3.9%, while in high-risk populations, such as war veterans, it can be as high as 30%. As a key pathway connecting the central nervous system to peripheral organs, the gut-brain axis has received increasing attention for its role in PTSD. Although the gut-brain axis has been shown to be associated with several psychiatric disorders, especially depression, its specific role in PTSD remains undercharacterized. Existing studies suggest that specific strains of Lactobacillus (e.g., Lactobacillus reuteri) may alleviate inflammatory responses and improve PTSD-like behaviors by down-regulating the expression of pro-inflammatory factors (IL-6 and TNF-α). In this study, we used a narrative review approach to sort out the research progress of gut microbiota alteration in PTSD, and compared the characteristics of changes in specific microbial taxa (e.g., Bacteroides, Lactobacillus, etc.), the index of microbiota diversity (α/β diversity), and the levels of inflammatory markers (e.g., IL-6, TNF-α) between the animal model and the human patients, respectively, in order to We further explored the potential pathogenic mechanisms mediated by microorganisms, such as influencing the vagal pathway, hypothalamic-pituitary-adrenal (HPA) axis function, immune system and other processes involved in the pathology of PTSD, and summarized the intervention strategies targeting gut microecology, such as probiotic supplementation, dietary interventions and fecal bacteria transplantation.
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Neurological and Psychiatric Adverse Effects of Antimicrobials.
Antimicrobials are a widely used class of medications, but several of them are associated with neurological and psychiatric side effects. The exact incidence of neurotoxicity with anti-infectives is unknown, although it is estimated to be < 1%. Neurotoxicity occurs with all classes of antimicrobials, such as antibiotics, antimycobacterials, antivirals, antifungals and antiretrovirals, with side effects ranging from headaches, anxiety and depression to confusion, delirium, psychosis, mania and seizures, among others. It is important to consider these possible side effects to prevent misdiagnosis or delayed treatment as drug withdrawal can be associated with reversibility in most cases. This article highlights the different neurotoxic effects of a range of antimicrobials, discusses proposed mechanisms of onset and offers general management recommendations. The effects of antibiotics on the gut microbiome and how they may ultimately affect cognition is also briefly examined.
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Research Progress on the Pathogenesis of Post-Stroke Depression.
Poststroke depression (PSD) is a common neuropsychiatric complication following stroke. Clinically, it is characterized by persistent low mood, cognitive dysfunction, and somatic symptoms, which severely impact the recovery and quality of life of stroke patients, making it an urgent issue in clinical practice. Currently, the pathogenesis of PSD remains incompletely understood. This study presents a narrative review of the literature from PubMed, Web of Science, and CNKI, with a particular focus on research conducted between 2021 and 2025. The findings reveal that advancements in neuroscience, immunology, and gut microbiome studies have contributed to important breakthroughs in understanding the mechanisms underlying PSD, such as the interaction between the hypothalamic-pituitary-adrenal (HPA) axis and neuroinflammation. In terms of treatment, several novel approaches have emerged. Traditional Chinese medicine (TCM) has attracted increasing attention due to its low cost, high safety, and minimal side effects. Herbal formulas have shown promising therapeutic effects for PSD. Moreover, combination therapies, such as acupuncture combined with repetitive transcranial magnetic stimulation (rTMS), have been demonstrated to be more effective than monotherapies. This review summarizes the multidimensional pathophysiology of PSD, including neurotransmitter imbalance, neuroinflammation, impaired neuroplasticity, structural brain damage, HPA axis dysregulation, gut-brain axis imbalance, and psychosocial factors. Additionally, current clinical treatment strategies for PSD are reviewed, with the aim of providing a theoretical foundation for early diagnosis, timely intervention, the development of novel anti-PSD therapies, and the establishment of more comprehensive treatment strategies for PSD.
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Microbial glutamate metabolism predicts intravenous cocaine self-administration in diversity outbred mice.
The gut microbiome is thought to play a critical role in the onset and development of psychiatric disorders, including depression and substance use disorder (SUD). To test the hypothesis that the microbiome affects addiction predisposing behaviors and cocaine intravenous self-administration (IVSA) and to identify specific microbes involved in the relationship, we performed 16S rRNA gene sequencing on feces from 228 diversity outbred mice. Twelve open field measures, two light-dark assay measures, one hole board and novelty place preference measure significantly differed between mice that acquired cocaine IVSA (ACQ) and those that failed to acquire IVSA (FACQ). We found that ACQ mice are more active and exploratory and display decreased fear than FACQ mice. The microbial abundances that differentiated ACQ from FACQ mice were an increased abundance of Barnesiella, Ruminococcus, and Robinsoniella and decreased Clostridium IV in ACQ mice. There was a sex-specific correlation between ACQ and microbial abundance, a reduced Lactobacillus abundance in ACQ male mice, and a decreased Blautia abundance in female ACQ mice. The abundance of Robinsoniella was correlated, and Clostridium IV inversely correlated with the number of doses of cocaine self-administered during acquisition. Functional analysis of the microbiome composition of a subset of mice suggested that gut-brain modules encoding glutamate metabolism genes are associated with the propensity to self-administer cocaine. These findings establish associations between the microbiome composition and glutamate metabolic potential and the ability to acquire cocaine IVSA thus indicating the potential translational impact of targeting the gut microbiome or microbial metabolites for treatment of SUD. This article is part of the Special Issue on "Microbiome & the Brain: Mechanisms & Maladies".
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Gut Biome and Mental Health: Do Probiotics Work?
Mental health conditions have been linked closely to an imbalance of microbiota in the gut, leading to disruption of the microbiome (dysbiosis). Several neurotransmitters, such as GABA (gamma-aminobutyric acid), serotonin, and glutamate, are produced in the gut, which are associated with anxiety and depressive symptoms. Mental health and the gut have been linked closely, and many mental illnesses have been associated with gut dysbiosis. Probiotics are marketed to improve gut health, act as mood enhancers, and be effective in reducing stress as unregulated over-the-counter supplements. Given healthcare disparities and patient-doctor gaps across the globe, this review aims to appraise the literature on probiotics for the prevention and treatment of mental disorders. PubMed and Google Scholar databases were searched till March 2023 using the MeSH words "prebiotics," "probiotics," "synbiotics," and "psychobiotics." Out of 207 studies, 26 studies met the inclusion criteria and were included in the review. Studies suggest probiotics could be an effective and economical adjunct therapy; however, due to weak study design and low power, the results are inconclusive. Their use is not without risks, and healthcare providers need close supervision until more robust longitudinal studies are conducted to appraise their efficacy and safety profiles.
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Obese-type gut microbiota induce neurobehavioral changes in the absence of obesity.
BACKGROUND: The prevalence of mental illness, particularly depression and dementia, is increased by obesity. Here, we test the hypothesis that obesity-associated changes in gut microbiota are intrinsically able to impair neurocognitive behavior in mice. METHODS: Conventionally housed, nonobese, adult male C57BL/6 mice maintained on a normal chow diet were subjected to a microbiome depletion/transplantation paradigm using microbiota isolated from donors on either a high-fat diet (HFD) or control diet. Following re-colonization, mice were subjected to comprehensive behavioral and biochemical analyses. RESULTS: The mice given HFD microbiota had significant and selective disruptions in exploratory, cognitive, and stereotypical behavior compared with mice with control diet microbiota in the absence of significant differences in body weight. Sequencing-based phylogenetic analysis confirmed the presence of distinct core microbiota between groups, with alterations in α- and β-diversity, modulation in taxonomic distribution, and statistically significant alterations to metabolically active taxa. HFD microbiota also disrupted markers of intestinal barrier function, increased circulating endotoxin, and increased lymphocyte expression of ionized calcium-binding adapter molecule 1, toll-like receptor 2, and toll-like receptor 4. Finally, evaluation of brain homogenates revealed that HFD-shaped microbiota increased neuroinflammation and disrupted cerebrovascular homeostasis. CONCLUSIONS: Collectively, these data reinforce the link between gut dysbiosis and neurologic dysfunction and suggest that dietary and/or pharmacologic manipulation of gut microbiota could attenuate the neurologic complications of obesity.
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Environmental risk factors for inflammatory bowel disease.
Crohn's disease (CD) and ulcerative colitis (UC) are chronic immunologically mediated diseases that often have a relapsing-remitting course in young persons. Genetic-risk polymorphisms explain less than one third of the heritability of disease. Epidemiologic and laboratory data suggest that environmental factors play a significant role in influencing the risk and natural history of disease. Smoking is the most widely and consistently described risk factor. It, however, increases the risk of CD while conferring protection against UC. The gut microbiome is a key component in the development of inflammatory bowel disease (IBD). Several external factors potentially exert an effect by influencing the composition of the gut microbiome or disrupting the intestinal barrier. These external influences include the use of antibiotics or nonsteroidal anti-inflammatory drugs and the presence of enteric infections. Data on diet have been inconsistent, but high fiber intake, particularly of soluble fiber, appears to protect against CD, whereas protein intake may increase disease risk. Vitamin D may also play an important protective role, particularly in patients with CD. Neurobehavioral factors, such as stress and depression, also influence the risk of IBD. Systematic and rigorous studies of environmental exposures in the management of IBD are needed. In particular, studies of whether environmental factors can be modified to reduce the likelihood of relapse or improve patient outcomes would be valuable.
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Gut microbial and human genetic signatures of inflammatory bowel disease increase risk of comorbid mental disorders.
The high prevalence of comorbid mental disorders (CMDs) in patients with inflammatory bowel disease (IBD) is well-documented. This study delves into the intricate CMD-IBD relationship through comprehensive analyses using human variants, gut microbiome, and anxiety/depression estimates from a cohort of 507 IBD patients and 75 controls. Notably, patients with IBD, especially those with CMD, exhibited lower diversity than controls. We identified 106 differentially abundant taxa (DATs) in IBD patients compared to controls and 21 DATs distinguishing CMD-affected from CMD-free IBD patients. Microbial IBD-risk scores, reflecting an individual's microbial burden for IBD, revealed a significant enrichment of IBD-risk signatures in CMD-affected patients compared to CMD-free patients. Additionally, there was an IBD-risk variant potentially regulating the abundance of an IBD/CMD-associated DAT, suggesting an interplay between IBD-risk variants and dysbiosis in CMD. Our investigation underscores the pivotal role of IBD-associated gut dysbiosis in predisposing IBD patients to CMD, partially through genetic variant-mediated mechanisms.
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Choline metabolism in regulating inflammatory bowel disease-linked anxiety disorders: A multi-omics exploration of the gut-brain axis.
Anxiety and depression caused by inflammatory bowel disease (IBD) negatively affect the mental health of patients. Emerging studies have demonstrated that the gut-brain axis (GBA) mediates IBD-induced mood disorders, but the underlying mechanisms of these findings remain unknown. Therefore, it's vital to conduct comprehensive research on the GBA in IBD. Multi-omics studies can provide an understanding of the pathological mechanisms of the GBA in the development of IBD, helping to uncover the mechanisms underlying the onset and progression of the disease. Thus, we analyzed the prefrontal cortex (PFC) of Dextran Sulfate Sodium Salt (DSS)-induced IBD mice using transcriptomics and metabolomics. We observed increased mRNA related to acetylcholine synthesis and secretion, along with decreased phosphatidylcholine (PC) levels in the PFC of DSS group compared to the control group. Fecal metagenomics also revealed abnormalities in the microbiome and lipid metabolism in the DSS group. Since both acetylcholine and PC are choline metabolites, we posited that the DSS group may experience choline deficiency and choline metabolism disorders. Subsequently, when we supplemented CDP-choline, IBD mice exhibited improvements, including decreased anxiety-like behaviors, reduced PC degradation, and increased acetylcholine synthesis in the PFC. In addition, administration of CDP-choline can restore imbalances in the gut microbiome and disruptions in lipid metabolism caused by DSS treatment. This study provides compelling evidence to suggest that choline metabolism plays a crucial role in the development and treatment of mood disorders in IBD. Choline and its metabolites appear to have a significant role in maintaining the stability of the GBA.
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Personality Affects Zebrafish Response to Sertraline.
Sertraline is widely prescribed to treat anxiety and depression. Sertraline acts by blocking serotonin, norepinephrine, and dopamine transporters systems and has been detected in surface waters globally, where it may impact fish behavior. We classified zebrafish personality on three behavioral axes, boldness, anxiety, and sociability, assigning fish as either high or low in each category. The fish were exposed to nominal concentrations of 0, 5, 50, 500, or 5000 ng/L sertraline (measured concentrations: <10, 21.3, 370, and 2200 ng/L, respectively) to assess changes in boldness, anxiety, and sociability after 7 and 28 days. We also measured shoaling behavior and response to an alarm cue, and determined the gut microbiome of a subset of fish. After 7 days there was no overall effect of sertraline on boldness, but there was an interaction between initial personality and sex, with a stronger impact on females classified as low-boldness personality. Sertraline reduced sociability in all treatments compared with the control, but there was again an interaction between sertraline and initial personality. Fish that were classified as low-sociability responded more strongly to sertraline. After 7 days, fish exposed to a nominal concentration of 5000 ng/L (2200 ng/L measured) showed higher anxiety than controls, with the overall pattern of initial behavior retained. After 28 days, similar patterns were observed, but with higher variation. There was only a weak association between the gut microbiome and personality. Overall, the study highlights the importance of considering initial behavior, which can affect response to pollutants. Our results may also be applicable to human studies and provide a mechanism to explain why different individuals respond differently to the drug. Environ Toxicol Chem 2024;43:132-146. © 2023 SETAC.