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Microbiota and parasite relationship.
The diversity of microbiota is different in each person. Many health problems such as autoimmune diseases, diabetes, cardiovascular diseases, and depression can be caused by microbiota imbalance. Since the parasite needs a host to survive, it interacts closely with the microbiota elements. Blastocystis acts on the inflammatory state of the intestine and may cause various gastrointestinal symptoms, on the contrary, it is more important for gut health because it causes bacterial diversity and richness. Blastocystis is associated with changes in gut microbiota composition, the ultimate indicator of which is the Firmicutes/Bacteroidetes ratio. The Bifidobacterium genus was significantly reduced in IBS patients and Blastocystis, and there is a significant decrease in Faecalibacterium prausnitzii, which has anti-inflammatory properties in Blastocystis infection without IBS. Lactobacillus species reduce the presence of Giardia, and the produced bacteriocins prevent parasite adhesion. The presence of helminths has been strongly associated with the transition from Bacteroidetes to Firmicutes and Clostridia. Contrary to Ascaris, alpha diversity in the intestinal microbiota decreases in chronic Trichuris muris infection, and growth and nutrient metabolism efficiency can be suppressed. Helminth infections indirectly affect mood and behavior in children through their effects on microbiota change. The main and focus of this review is to address the relationship of parasites with microbiota elements and to review the data about what changes they cause. Microbiota studies have gained importance recently and it is thought that it will contribute to the treatment of many diseases as well as in the fight against parasitic diseases in the future.
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Intricate mechanism of anxiety disorder, recognizing the potential role of gut microbiota and therapeutic interventions.
Anxiety is a widespread psychological disorder affecting both humans and animals. It is a typical stress reaction; however, its longer persistence can cause severe health disorders affecting the day-to-day life activities of individuals. An intriguing facet of the anxiety-related disorder can be addressed better by investigating the role of neurotransmitters in regulating emotions, provoking anxiety, analyzing the cross-talks between neurotransmitters, and, most importantly, identifying the biomarkers of the anxiety. Recent years have witnessed the potential role of the gut microbiota in human health and disorders, including anxiety. Animal models are commonly used to study anxiety disorder as they offer a simpler and more controlled environment than humans. Ultimately, developing new strategies for diagnosing and treating anxiety is of paramount interest to medical scientists. Altogether, this review article shall highlight the intricate mechanisms of anxiety while emphasizing the emerging role of gut microbiota in regulating metabolic pathways through various interaction networks in the host. In addition, the review will foster information about the therapeutic interventions of the anxiety and related disorder.
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Tryptophan Metabolism Disorder-Triggered Diseases, Mechanisms, and Therapeutic Strategies: A Scientometric Review.
BACKGROUND: Tryptophan is widely present in foods such as peanuts, milk, and bananas, playing a crucial role in maintaining metabolic homeostasis in health and disease. Tryptophan metabolism is involved in the development and progression of immune, nervous, and digestive system diseases. Although some excellent reviews on tryptophan metabolism exist, there has been no systematic scientometric study as of yet. METHODS: This review provides and summarizes research hotspots and potential future directions by analyzing annual publications, topics, keywords, and highly cited papers sourced from Web of Science spanning 1964 to 2022. RESULTS: This review provides a scientometric overview of tryptophan metabolism disorder-triggered diseases, mechanisms, and therapeutic strategies. CONCLUSIONS: The gut microbiota regulates gut permeability, inflammation, and host immunity by directly converting tryptophan to indole and its derivatives. Gut microbial metabolites regulate tryptophan metabolism by activating specific receptors or enzymes. Additionally, the kynurenine (KYN) pathway, activated by indoleamine-2, 3-dioxygenase (IDO) and tryptophan 2, 3-dioxygenase, affects the migration and invasion of glioma cells and the development of COVID-19 and depression. The research and development of IDO inhibitors help to improve the effectiveness of immunotherapy. Tryptophan metabolites as potential markers are used for disease therapy, guiding clinical decision-making. Tryptophan metabolites serve as targets to provide a new promising strategy for neuroprotective/neurotoxic imbalance affecting brain structure and function. In summary, this review provides valuable guidance for the basic research and clinical application of tryptophan metabolism.
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Akkermansia muciniphila Protects Against Psychological Disorder-Induced Gut Microbiota-Mediated Colonic Mucosal Barrier Damage and Aggravation of Colitis.
Psychological disorders are associated with increased risk of severe inflammatory bowel disease (IBD) by causing gut microbiota dysbiosis and colonic mucosal barrier damage. However, the interaction between chronic restraint stress (CRS), gut microbiota composition, and colonic mucus remains unclear. We demonstrated that mice under CRS conditions exhibited alterations in microbiota composition, disruption of colonic mucus, and aggravation of colitis. In addition, the abundance of Akkermansia muciniphila was significantly decreased in mice under CRS and UC patients with depression, and positively associated with the expression of MUC2. After antibiotic treatment, the recipient mice colonized with CRS microbiota showed barrier defects and severe colitis. Administration of Akkermansia muciniphila was found to restore colonic mucus and modify the gut microbiota. We confirm that CRS-mediated gut microbiota dysbiosis results in colonic mucosal barrier damage and aggravation of colitis. Our results suggest that A. muciniphila is expected to be a potential probiotic to protect and treat colonic mucus that is involved in IBD with psychological disorders.
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Symptomatologic outcomes of gut microbiota modifiers (probiotics, prebiotics and synbiotics) in cancer care: A scoping review of randomized controlled trials.
BACKGROUND: Microbiota modifiers offer potential benefits for improving the wide spectrum of symptoms and clinical outcomes in individuals with cancer. However, there is a lack of comprehensive literature mapping to determine which specific cancer and treatment-related symptoms have been investigated as potential targets for gut microbiota modifiers. This scoping review aims to systematically analyze clinical trials on microbiota modifiers in managing cancer and treatment-related symptoms in adults. METHODS: We conducted a scoping review of randomized controlled trials (RCTs) across four databases up to May 2025, following our published protocol and JBI principles with PRISMA 2020 guidelines. RESULTS: The literature review identified 33 eligible studies, primarily involving patients with pelvic cancers. The most common outcomes examined in the clinical trials were gastrointestinal symptoms. Other studies focused on patients with head, neck, and breast cancer, examining quality of life, mucositis, fatigue, anxiety, depression, and the use of rescue drugs. CONCLUSION: Despite evidence of potential benefits for gastrointestinal symptoms, inconsistent findings across studies warrant further well-designed, large-scale research to understand probiotics' effectiveness and mechanisms.
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Sodium Butyrate Protects the Intestinal Barrier by Modulating Intestinal Host Defense Peptide Expression and Gut Microbiota after a Challenge with Deoxynivalenol in Weaned Piglets.
This study aims to determine whether sodium butyrate (SB) could antagonize deoxynivalenol (DON)-induced intestinal epithelial dysfunction. In a four-week feeding trial, twenty-eight barrows were randomly divided into four treatments: (1) uncontaminated basal diet (control); (2) 4 mg/kg DON-contaminated diet (DON); (3) basal diet supplemented with 0.2% SB (SB); and (4) 4 mg/kg DON + 0.2% SB (DON + SB). A decrease in performance was observed in DON-exposed animals, which was prevented by the dietary SB supplementation. DON exposure also depressed the expression of host defense peptides (HDPs) in the intestine, impaired the intestinal barrier integrity, and disturbed the gut microbiota homeostasis. These alterations induced by DON were attenuated by SB supplementation. The supplementation of 0.2% SB ameliorated the adverse effects of DON on the liver in terms of hepatic lesions as well as serum concentrations of alkaline phosphatase and aspartate aminotransferase. In IPEC-J2 cells, pretreatment with SB alleviated the DON-induced decreased cell viability. Additionally, the NOD2/caspase-12 pathway participated in the alleviation of SB on DON-induced diminished HDP expression. Taken together, these data demonstrated that SB protected piglets from DON-induced intestinal barrier dysfunction potentially through stimulation of intestinal HDP assembly and regulation in gut microbiota.
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Mechanism-First Psychobiotics: Fermented Vegetables, Dairy, and Soy for Depression and Anxiety.
Depression and anxiety are increasingly understood to involve systemic biological processes, where chronic stress, immune dysregulation, and vascular dysfunction converge on brain-relevant symptoms. Fermented foods are widely studied as psychobiotic candidates, yet results remain inconsistent because products vary in chemistry, viability, sodium, and biogenic amines, and trials often rely on broad symptom outcomes without exposure verification. A major gap is the lack of a reusable, mechanism-first framework that links what a product delivers to barrier, endothelial, and neurovascular target engagement. As a narrative and conceptual review rather than a systematic review, the article integrates mechanistic evidence into a conceptual framework rather than undertaking quantitative evidence synthesis. It addresses that gap by treating fermented vegetables, dairy, soy, and selected Brazilian cassava ferments and artisanal cheeses as metabolite-engineering platforms mapped onto a tri-barrier remodeling axis from gut epithelium to endothelium and platelets to the blood-brain barrier. We synthesize dosing-resolved metabolite modules, including short-chain fatty acids, tryptophan-derived indoles, bile acids, neuroactive small molecules, and peptide and exopolysaccharide fingerprints, and align them with interpretable readouts for permeability, endotoxemia proxies, endothelial activation, immunothrombosis, and epigenetic aging pace. Here we highlight how this modular framework converts heterogeneous food studies into testable exposure hypotheses, guides comparator design and phenotype stratification, and clarifies why null results can be informative. To maintain a focused scope, the review uses selected fermented-food families as representative test platforms rather than attempting a complete survey of global fermented foods. The emphasis is therefore placed on mechanisms, exposure verification, and trial-design principles that can be transferred to other products.
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Investigating the Effect of Capric Acid on Antibiotic-Induced Autism-Like Behavior in Rodents.
Owing to the high prevalence of gastrointestinal dysfunction in patients, the gut-brain axis is considered to play a vital role in neurodevelopment diseases. Recent pieces of evidence have pointed to the usage of antibiotics at an early developmental stage to be a causative factor in autism due to its ability to induce critical changes in the gut microbiota. The purpose of the study is to determine the neuroprotective effect of capric acid (CA) on autism in antibiotic-induced gut dysbiosis in rodents. In this study, the effect of CA was observed in penicillin V (31 mg/kg, p.o.) exposed animals by evaluating their autism-like behavioral and biochemical parameters. The establishment of gut dysbiosis was confirmed by 16 RNA sequencing, and behavioral tests were performed. Subsequently, oxidative stress, cytokine levels, and mitochondrial complex activities in the hippocampus and prefrontal cortex were analyzed. It was observed that the administration of penicillin V during the perinatal period produced gut dysbiosis and long-lasting changes in social behavior with symptoms of anxiety and depression and impaired learning and memory. Treatment with penicillin V also produced oxidative stress, mitochondrial dysfunction, and inflammation in the hippocampus and prefrontal cortex. Treatment with CA produced a positive effect on the alterations with maximum effects evident at 400 mg/kg, p.o. through amelioration of behavioral as well as biochemical changes. The current study concluded that CA could act as a likely candidate for the treatment and management of autism via modulation of gut dysbiosis-induced neurobehavioral parameters, oxidative stress, mitochondrial dysfunction, and inflammatory markers.
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The impact of a high-fat diet (HFD) on mouse behavior, neurotransmitters, inflammation, and gut-brain axis metabolism under hypoxic conditions.
In the context of the increasing global prevalence of mental health disorders, depression and anxiety have emerged as significant public health challenges. Notably, the incidence rates are higher in plateau regions. This study aimed to investigate the effects and underlying mechanisms of a high-fat diet (HFD) and hypoxic conditions on mouse behavior. The mice were subjected to different diets (a HFD or a normal diet) and placed in a hypoxic environment. This study explored relevant mechanisms through the measurement of physical and behavioral indicators, pathological assessments, biochemical analyses, evaluation of gut microbiota diversity, and metabolomics. The results indicated that a HFD induced obesity in mice under hypoxic conditions, leading to abnormal behavior and reduced synthesis of neurotransmitters such as 5-hydroxytryptaminergic (5-HT), norepinephrine (NE), dopamine (DA), and gamma-aminobutyric acid (GABA). Additionally, a HFD may synergize with increased hypoxia-inducible factor (HIF) expression under hypoxic conditions, exacerbating multitissue inflammation, increasing proinflammatory factor levels, decreasing anti-inflammatory factor levels, and causing systemic inflammation due to gut injury, thereby damaging brain and gut tissues. Furthermore, a HFD altered the gut microbiota diversity, reducing beneficial bacteria while increasing harmful bacteria. KEGG pathway analysis and metabolomics revealed that the brain-gut metabolic pathway clustered around kynurenine metabolism, with metabolites such as kynurenic acid, 2-oxoadipic acid, (2-oxo-2,3-dihydro-1h-indol-3-yl) acetic acid, and D-kynurenine being reduced, which are associated with inflammatory and depressive/anxious behaviors. Subsequent Spearman correlation analysis revealed an interaction network among all factors, with kynurenic acid positioned at the core, serving as a key hub for interactions. Under dual stimulation from hypoxia and a HFD, this network becomes imbalanced, inducing cerebral and gut metabolic disorders and abnormal behaviors. This study elucidates the multifactorial mechanisms underlying abnormal behavior caused by a HFD and hypoxia in mice, providing a foundation for future research and prevention and treatment strategies for mental health disorders in plateau regions.
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The intake of pulses and vegetables is associated with an increase in the Lachnospira abundance and a decrease in stress: Analysis of the 'Sukoyaka Health Survey'.
Stress negatively affects physical and mental health, leading to conditions like depression and anxiety. Diet and gut microbiota are crucial factors influencing stress and mental health. We hypothesized that not a single nutrient but a combination of nutrients affects stress response via gut microbiota. This study investigated the relationships among diet quality, gut microbiota, and stress in healthy adults, specifically examining the associations between Nutrient Rich Food index 9.3 (NRF9.3) scores, gut microbiota, and stress responses. Data were collected from the "Sukoyaka Health Survey," which included the Food Frequency Questionnaire (FFQ), Brief Job Stress Questionnaire (BJSQ), and gut microbiota analysis of 1058 participants. Stress scores were calculated using the BJSQ, and diet quality was assessed using the NRF9.3. Cluster analysis was used to create clusters based on stress scores, and diet and gut microbiota were compared between clusters. A probabilistic network modeling was used to evaluate the relationships among diet, gut microbiota, and stress. Participants with higher stress scores had lower NRF9.3 scores and altered gut microbiota, particularly a lower abundance of Lachnospira. Foods like natto, tomatoes, and green peppers were consumed less by the high-stress group. Using exploratory probabilistic network modeling, our analysis predicted that higher consumption of these foods was associated with an increase in the NRF9.3 score and may reduce stress by enhancing Lachnospira abundance. These findings suggest that the consumption of natto, tomatoes, and green peppers may contribute to increasing NRF9.3 scores and the abundance of Lachnospira, and potentially decreasing the physical and mental stress response scores.