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Signatures of HIV and Major Depressive Disorder in the Plasma Microbiome.
Inter-individual differences in the gut microbiome are linked to alterations in inflammation and blood-brain barrier permeability, which may increase the risk of depression in people with HIV (PWH). The microbiome profile of blood, which is considered by many to be typically sterile, remains largely unexplored. We aimed to characterize the blood plasma microbiome composition and assess its association with major depressive disorder (MDD) in PWH and people without HIV (PWoH). In this cross-sectional, observational cohort, we used shallow-shotgun metagenomic sequencing to characterize the plasma microbiome of 151 participants (84 PWH and 67 PWoH), all of whom underwent a comprehensive neuropsychiatric assessment. The microbial composition did not differ between PWH and PWoH or between participants with MDD and those without it. Using the songbird model, we computed the log ratio of the highest and lowest 30% of the ranked classes associated with HIV and MDD. We found that HIV infection and lifetime MDD were enriched in a set of differentially abundant inflammatory classes, such as Flavobacteria and Nitrospira. Our results suggest that the circulating plasma microbiome may increase the risk of MDD related to dysbiosis-induced inflammation in PWH. If confirmed, these findings may indicate new biological mechanisms that could be targeted to improve treatment of MDD in PWH.
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A Scoping Review of the Positive and Negative Bacteria Associated With the Gut Microbiomes of Systemic Lupus Erythematosus Patients.
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that affects multiple systems of the body. Recent research on the gut microbiota dysbiosis associated with SLE patients has gained traction and warranted further exploration. It has not been determined whether the change in the gut microbiota is a cause of SLE or a symptom of SLE. However, based on the physiological and pathophysiological role of the bacteria in the gut microbiome, as levels of the bacteria rise or fall, symptomatology in SLE patients could be affected. This review analyzes the recent studies that examined the changes in the gut microbiota of SLE patients and highlights the correlations between gut dysbiosis and the clinical manifestations of SLE. A systematic search strategy was developed by combining the terms "SLE," "systemic lupus erythematosus," and "gut microbiome." Biomedical Reference Collection, CINAHL, Medline ProQuest, and PubMed Central databases were searched by combining the appropriate keywords with "AND." Only full-text, English-language articles were searched. The articles were restricted from 2013 to 2023. Only peer-reviewed controlled studies with both human and animal trials were included in this scoping review. Review articles, non-English articles, editorials, case studies, and duplicate articles from the four databases were excluded. Various species of bacteria were found to be positively or negatively associated with SLE gut microbiomes. Among the bacterial species increased were Clostridium, Lactobacilli, Streptococcus, Enterobacter, and Klebsiella. The bacterial species that decreased were Bifidobacteria, Prevotella, and the Firmicutes/Bacteroidetes ratio. Literature shows that Clostridium is one of several bacteria found in abundance, from pre-disease to the diseased state of SLE. Lachnospiraceae and Ruminococcaceae are both part of the family of butyrate-producing anaerobes that are known for their role in strengthening the skin barrier function and, therefore, may explain the cutaneous manifestations of SLE patients. Studies have also shown that the Firmicutes/Bacteroidetes ratio is significantly depressed, which may lead to appetite changes and weight loss seen in SLE patients. Based on the established role of these bacteria within the gut microbiome, the disruption in the gut ecosystem could explain the symptomatology common in SLE patients. By addressing these changes, our scoping review encourages further research to establish a true causal relationship between the bacterial changes in SLE patients as well as furthering the scope of microbiota changes in other systems and autoimmune diseases.
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Evaluation of the clinical efficacy of Pediococcus acidilactici CCFM6432 in alleviating depression.
Aim: Accumulating evidence highlights the crucial role of the "gut-brain axis" and emphasizes the potential of dietary interventions to improve brain health through this pathway. This study assesses the effects of the probiotic Pediococcus acidilactici CCFM6432 on mood, sleep, and gastrointestinal function in patients with depressive disorder. Methods: This clinical trial is a randomized, placebo-controlled study (Registration: ChiCTR2300071025). It enrolled 39 adult patients diagnosed with depressive disorder, who were randomly assigned to either the placebo control group (n = 19) or the CCFM6432 intervention group (n = 20). The intervention period spanned four weeks. Assessments were conducted at both the beginning and end of the trial, including comprehensive questionnaire evaluations and the collection of serum and fecal samples. Results: In comparison to the placebo, treatment with CCFM6432 significantly decreased depression and anxiety scores, as well as ameliorated gastrointestinal dysfunction and poor sleep quality commonly associated with mood disorders. Microbiota analysis revealed an increase in species richness without notable changes in overall diversity, yet Pediococcus species was found to be more abundant post-treatment. Functional analysis indicated reduced activity in the NOD-like receptor signaling pathway, suggesting anti-inflammatory effects induced by the probiotic. Metabolomic profiling identified elevated levels of fecal lactic acid, which correlated with lower Hospital Anxiety and Depression Scale (HADS) scores, thereby linking probiotic metabolism to mood enhancement. Conclusion: These findings imply that CCFM6432 may improve brain function by modulating gut microbiota and their mediated immune homeostasis, underscoring its potential as an adjunctive treatment for mental disorders.
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["Pseudoneurotransmission" and gut microbiome - brain communication in neuropsychiatric disorders].
The gut microbiome, which comprises symbiotic bacteria colonizing the human digestive tract, undergoes dynamic changes during the lifespan, as evidenced by the fact that the number of species and the diversity of their composition decrease significantly with age. The aim of this review is to illuminate bilateral neuroimmunological pathways that determine the role of gut microbiome dysbiosis, not only as a cause but also as a byproduct of many neurodegenerative diseases of the CNS, such as Alzheimer's disease (AD) and Parkinson's disease (PD), but also in the frame of several behavioral and psychiatric pathological conditions such as depressive and anxiety disorders, schizophrenia, and autism spectrum disorder (ASD). Dysbiosis, in particular, reveals a model of "deceptive" mimicry of host molecules that might cause abnormal folding ("misfolding") and pathological aggregation of Aβ-peptide, leading to its dispersion through the gut-brain axis, precipitating microglia cell activation. By controlling myelination at the prefrontal cortex (PFC), a crucial area for multifaceted cognitive behavior, forecasting, and decision-making, the gut/microbiome-brain axis influences mood and social behavior, since major depressive disorder is correlated to white matter disturbance in the PFC, due to disregulations in the expression of myelin-related mRNA in this area. The gut microbiome is altered in psychosis compared to healthy controls, while medication with antipsychotics may result in reduced microbial community diversity. The vagus nerve, as a key element of the parasympathetic nervous system, regulating immune responses, may "detect" gut microbiome metabolites and transfer this intestinal information to the CNS, through its afferents, as in a "pseudo-neurotransmission" process. Scientific interest towards microbiome-based therapies increases as psychobiotics (which are strains of probiotics/prebiotics with specific properties to influence the gut-brain axis) appear to be able to exercise a beneficial effect in many CNS disorders. Lifestyle modifications, such as dietary interventions via psychobiotics intake that might enhance the gut microbiome's ability to produce beneficial metabolites that exert therapeutic effects on intestinal permeability, cognitive function, and immunity, may reveal new research pathways and therapeutic directions leading to a radical change of the "epistemology paradigm" as far as prevention and treatment of major neuro-psychiatric disorders is concerned.
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The association between dietary exposures and anxiety symptoms: A prospective analysis of the Australian Longitudinal Study on Women's Health cohort.
BACKGROUND: Nutrition is a potentially modifiable risk factor for mental disorders. Since anxiety is the most common mental disorder globally and most commonly impacts women, understanding its relationship with dietary exposures may elucidate important prevention and treatment approaches. We aimed to explore the association between dietary exposures and incident anxiety in women. METHODS: We used prospective longitudinal dietary data from 20,307 women enrolled in the Australian Longitudinal Study on Women's Health from 1973 to 1978 (young cohort between waves 3-5) and 1946-1951 (mid cohort between waves 3-7). Dietary exposures were defined according to the Global Burden of Disease framework (from wave 3). The primary outcome, anxiety and secondary outcome, depression were measured using subscales of the Goldberg Anxiety and Depression Scale (from wave 4). Generalized estimating equation Poisson regression models estimated risk ratios with 95 % confidence intervals, adjusting for age, socioeconomic status, and energy intake. RESULTS: Higher intakes of vegetables (adjusted risk ratio [aRR]: 0.94, 95%CI: 0.93-0.96 per serve increase), fruits (aRR: 0.93, 95%CI: 0.92-0.94), nuts and seeds (aRR: 0.93, 95%CI: 0.89-0.98 per serve), milk (aRR: 0.98, 95%CI: 0.96 to 0.99 per serve), fiber (aRR: 0.76, 95%CI: 0.72 to 0.81 per 30-g) and calcium (aRR: 0.88, 95%CI: 0.84 to 0.91 per gram) were associated with lower risk of incident anxiety. Conversely, higher intake of processed meat (aRR: 1.02, 95%CI: 1.00-1.05 per serve) and sodium (aRR: 1.15, 95 % CI: 1.09-1.22 per 2-g) was associated with higher anxiety risk. CONCLUSIONS: Higher intake of plant-based foods and lower intake of processed foods may help reduce the risk of anxiety. Further prospective and intervention studies should confirm these associations and underlying biological mechanisms.
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Neuropsychiatric Disorders: Influence of Gut Microbe to Brain Signalling.
The microbiome gut brain (MGB) axis consists of bidirectional routes of communication between the gut and the brain. It has emerged as a potential therapeutic target for multiple medical specialties including psychiatry. Significant numbers of preclinical trials have taken place with some transitioning to clinical studies in more recent years. Some positive results have been reported secondary to probiotic administration in both healthy populations and specific patient groups. This review aims to summarise the current understanding of the MGB axis and the preclinical and clinical findings relevant to psychiatry. Significant differences have been identified between the microbiome of patients with a diagnosis of depressive disorder and healthy controls. Similar findings have occurred in patients diagnosed with bipolar affective disorder and irritable bowel syndrome. A probiotic containing Lactobacillus acidophilus, Lactobacillus casei, and Bifidobacterium bifidum produced a clinically measurable symptom improvement in patients with depressive disorder. To date, some promising results have suggested that probiotics could play a role in the treatment of stress-related psychiatric disease. However, more well-controlled clinical trials are required to determine which clinical conditions are likely to benefit most significantly from this novel approach.
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The Gut-Brain-Axis on the Manifestation of Depressive Symptoms in Epilepsy: An Evidence-Driven Hypothesis.
Epilepsy is a severe neurological disorder involving 70 million people around the globe. Epilepsy-related neuropsychiatric comorbidities such as depression, which is the most common, is an additional factor that negatively impacts the living quality of epilepsy patients. There are many theories and complexities associated with both epilepsy and associated comorbidities, one of which is the gut-brain-axis influence. The gut microbiome is hypothesized to be linked with many neurological disorders; however, little conclusive evidence is available in this area. Thus, highlighting the role will create interest in researchers to conduct detailed research in comprehending the influence of gut-brain-axis in the manifestation of depressive symptoms in epilepsy. The hypothesis which is explored in this review is that the gut-brain-axis do play an important role in the genesis of epilepsy and associated depression. The correction of this dysbiosis might be beneficial in treating both epilepsy and related depression. This hypothesis is illustrated through extensive literature discussion, proposed experimental models, and its applicability in the field. There is indirect evidence which revealed some specific bacterial strains that might cause depression in epilepsy.
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Altered gut microbial diversity, composition, and metabolomic potential in patients with major depressive disorder and recent suicide attempt.
This study investigates the role of the gut microbiome in suicidal behavior among individuals with major depressive disorder (MDD). Fecal samples from 50 hospitalized patients with MDD, including 35 with recent suicide attempts (60 % female) and 15 without a history of suicide (73 % female), were analyzed using 16S rRNA and shotgun sequencing to assess microbiome diversity and metabolic potential. Results revealed that suicide attempters exhibited significantly greater microbial richness and distinct beta-diversity patterns. Notably, they had higher levels of Fenollaria timonensis and lower levels of Corynebacterium aurimucosum. Additionally, 25 metabolic pathways differed between groups, with several linked to energy metabolism and amino acid processing-processes previously associated with MDD and suicidal behavior. These findings suggest that microbiome composition may influence suicide risk through gut-brain axis-mediated pathways, although due to the exploratory nature of this study further investigation is needed to validate our findings. Given the microbiome's modifiability, future research should explore microbial-targeted interventions as a potential strategy for suicide prevention in individuals with MDD.
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Protocol for a pilot randomised controlled trial of mindfulness-based cognitive therapy in youth with inflammatory bowel disease and depression.
INTRODUCTION: Inflammatory bowel disease (IBD) is a chronic autoinflammatory disease of the gastrointestinal tract with peak age of onset during adolescence and young adulthood. Adolescents and young adults (AYAs) with IBD experience higher depression rates compared with peers who are well or have other chronic conditions. Mindfulness-based interventions are of particular interest because of their potential to improve both the course of IBD and depression. METHODS AND ANALYSIS: This study is a parallel design, single-blind, pilot randomised controlled trial (RCT) of mindfulness-based cognitive therapy (MBCT) in AYAs with IBD and depression. The trial aims to recruit 64 participants who will be randomly allocated to MBCT or treatment as usual. The primary outcome measure is the depression subscale score from the Depression, Anxiety and Stress Scale. Secondary outcomes include anxiety, stress, post-traumatic growth, IBD-related quality of life, illness knowledge, medication adherence, mindfulness, IBD activity, inflammatory markers, microbiome and brain neuroconnectivity changes. All outcomes other than neuroimaging will be collected at three time points: at baseline, at therapy completion and at 20 weeks. Neuroimaging will be conducted at baseline and at therapy completion. Mixed-effects linear and logistic regression modelling will be used to analyse continuous and dichotomous outcomes, respectively. Participants' experiences will be explored through focus groups, and thematic analysis will be used to generate relevant themes. ETHICS AND DISSEMINATION: The protocol has been approved by the Mater Hospital Human Research Ethics Committee (HREC) and University of Queensland HREC. Trial findings will be published in peer-reviewed journals and will be presented at scientific conferences. TRIAL REGISTRATION NUMBER: ACTRN12617000876392, U1111-1197-7370; Pre-results.
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Global trends and future perspectives in autism spectrum disorder and gut microbiota research: a comprehensive bibliometric analysis.
BACKGROUND: Autism spectrum disorder (ASD) is a heterogeneous neurodevelopmental condition. Increasing studies examine whether gut microbiota alterations and the gut-brain axis are linked to ASD-relevant phenotypes. As the literature expands rapidly, a quantitative mapping is needed to clarify influential work and evolving themes. OBJECTIVE: To map global research on ASD and the gut microbiota, identify major contributors and knowledge bases, and characterize thematic evolution and emerging fronts. METHODS: We analyzed 1,391 English-language articles and reviews indexed in the Web of Science Core Collection (1999-2024). CiteSpace, VOSviewer, and R were used to evaluate publication trends, collaboration networks, co-citation structure, keyword clustering, and burst detection. RESULTS: Publication output increased slowly before 2010 and accelerated after 2018. The United States and China were leading contributors and key collaboration hubs. The co-citation core was anchored by landmark experimental and translational studies, including work on microbiome-to-behavior links and microbiome-targeted interventions. Keyword clustering and timeline views highlighted three prominent thematic directions: fecal microbiota transplantation, Rett syndrome, and maternal immune activation. Recurrent and burst keywords emphasized the gut-brain axis, short-chain fatty acids, gastrointestinal symptoms, and oxidative stress. Recent burst terms, including obesity, major depressive disorder, and glutamate, suggest increasing connections to metabolic and broader psychiatric dimensions. CONCLUSION: ASD-microbiome research has shifted from descriptive comparisons toward mechanism-oriented and intervention-relevant questions. Future progress will benefit from standardized protocols, longitudinal designs, and multi-omics integration, together with rigorously designed trials to evaluate microbiome-targeted strategies.