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Brain-Gut Axis Perspective on Irritable Bowel Syndrome: The Role of Gut Microbiota and Therapeutic Strategies of Traditional Chinese Medicine.
Irritable bowel syndrome (IBS) is one of the most common functional gastrointestinal disorders, with dysfunction of the gut-brain axis (GBA) being its core pathogenic mechanism. Traditional Chinese Medicine (TCM), guided by the theory of "liver-spleen interaction" and the core therapeutic principle of "soothing the liver and invigorating the spleen", has accumulated extensive clinical experience in IBS treatment. This review systematically searched PubMed, Web of Science, and CNKI databases to summarize the molecular mechanisms by which gut microbiota participate in IBS pathogenesis through the GBA, interpret the modern biological connotation of the TCM pathogenesis of "liver depression and spleen deficiency" from the perspective of the GBA, and review the evidence for TCM in treating IBS by modulating gut microbiota. The results indicate that gut microbiota dysbiosis drives IBS symptoms through three major metabolic pathways - short-chain fatty acids, bile acids, and 5-hydroxytryptamine - and achieves bidirectional regulation via the GBA. TCM monomers (e.g., berberine, curcumin, apigenin), single herbs (e.g., Atractylodes, Cinnamomum, Liupao tea), classical formulas (e.g., Tong-Xie-Yao-Fang, Chang-Kang-Fang, Si-Ni-San), as well as acupuncture and moxibustion, may improve IBS symptoms by restoring gut microbial diversity, regulating metabolite levels, repairing the intestinal barrier, and inhibiting inflammatory pathways. TCM may offer unique advantages in treating IBS through multi-target regulation of gut microbiota. Future research should focus on the objectification of TCM syndrome differentiation based on gut microbiota and the development of precision matching strategies.
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Microbiota metabolites modulate the T helper 17 to regulatory T cell (Th17/Treg) imbalance promoting resilience to stress-induced anxiety- and depressive-like behaviors.
Chronic stress disrupts immune homeostasis while gut microbiota-derived metabolites attenuate inflammation, thus promoting resilience to stress-induced immune and behavioral abnormalities. There are both peripheral and brain region-specific maladaptations of the immune response to chronic stress that produce interrelated mechanistic considerations required for the design of novel therapeutic strategies for prevention of stress-induced psychological impairment. This study shows that a combination of probiotics and polyphenol-rich prebiotics, a synbiotic, attenuates the chronic-stress induced inflammatory responses in the ileum and the prefrontal cortex promoting resilience to the consequent depressive- and anxiety-like behaviors in male mice. Pharmacokinetic studies revealed that this effect may be attributed to specific synbiotic-produced metabolites including 4-hydroxyphenylpropionic, 4-hydroxyphenylacetic acid and caffeic acid. Using a model of chronic unpredictable stress, behavioral abnormalities were associated to strong immune cell activation and recruitment in the ileum while inflammasome pathways were implicated in the prefrontal cortex and hippocampus. Chronic stress also upregulated the ratio of activated proinflammatory T helper 17 (Th17) to regulatory T cells (Treg) in the liver and ileum and it was predicted with ingenuity pathway analysis that the aryl hydrocarbon receptor (AHR) could be driving the synbiotic's effect on the ileum's inflammatory response to stress. Synbiotic treatment indiscriminately attenuated the stress-induced immune and behavioral aberrations in both the ileum and the brain while in a gut-immune co-culture model, the synbiotic-specific metabolites promoted anti-inflammatory activity through the AHR. Overall, this study characterizes a novel synbiotic treatment for chronic-stress induced behavioral impairments while defining a putative mechanism of gut-microbiota host interaction for modulating the peripheral and brain immune systems.
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Efficacy and safety of fecal microbiota transplantation for the treatment of diseases other than Clostridium difficile infection: a systematic review and meta-analysis.
The intestinal microbiome has been identified as a key modifier for a variety of health conditions. Fecal Microbiota Transplantation (FMT) has emerged as a fast, safe, and effective means by which to modify the intestinal microbiome and potentially treat a variety of health conditions. Despite extensive research of FMT for CDI, there is a lack of clarity informed by systematic synthesis of data regarding the safety and efficacy of FMT for other health conditions. This systematic review used PRISMA guidelines and was prospectively registered with PROSPERO (CRD42018104243). In March 2020, a search of MEDLINE, EMBASE, and PsycINFO was conducted. We identified 26 eligible studies. A meta-analysis of FMT for active Ulcerative Colitis (UC) showed that FMT significantly improved rates of clinical remission (OR = 3.634, 95% CI = 1.940 to 6.808, I2 = 0%, p < .001), clinical response (OR = 2.634, 95% CI = 1.441 to 4.815, I2 = 33%, p = .002) and endoscopic remission (OR = 4.431, 95% CI = 1.901 to 10.324, I2 = 0%, p = .001). With respect to Irritable Bowel Syndrome, a meta-analysis showed no significant change in symptoms following FMT (p = .739). Hepatic disorders, metabolic syndrome, and antibiotic-resistant organisms were conditions with emerging data on FMT. Serious adverse events (AE) were more often reported in control group participants (n = 43) compared with FMT group participants (n = 26). There were similar rates of mild to moderate AE in both groups. Preliminary data suggest that FMT is a potentially safe, well-tolerated and efficacious treatment for certain conditions other than CDI, with evidence for active UC being the most compelling.
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The liver-gut-brain axis in metabolic dysfunction-associated steatotic liver disease: bidirectional communication, clinical implications, and future perspectives.
BACKGROUND: Metabolic dysfunction-associated steatotic liver disease (MASLD) affects approximately one-third of adults worldwide and is increasingly recognized as a multisystem disorder. In addition to hepatic and cardiometabolic complications, many patients report fatigue, depression, anxiety, sleep disturbance, and subjective cognitive complaints. These manifestations are clinically important but correlate inconsistently with liver histology and may arise from several interacting mechanisms. AIM: To critically synthesize evidence on the liver-gut-brain axis in MASLD, distinguish established pathways from indirect or preclinical hypotheses, and evaluate implications for biomarkers, patient assessment, and treatment. METHODS: PubMed was searched through July 15, 2026 using combinations of terms related to MASLD/MASH, intestinal barrier function, gut microbiota, autonomic and stress signaling, hepatic inflammation and fibrosis, neuroinflammation, cognition, biomarkers, and treatment. Guidelines, randomized trials, prospective human studies, systematic reviews, and mechanistically informative experimental studies were prioritized. Evidence derived from cirrhosis, hepatic encephalopathy, other diseases, or animal models is explicitly identified. RESULTS: The axis comprises neural, endocrine, immune, and metabolic communication. Stress-related hypothalamic-pituitary-adrenal and sympathetic activation may influence behavior, adipose tissue, intestinal motility, mucosal immunity, and epithelial integrity. Barrier dysfunction can increase portal exposure to microbial products that activate hepatic inflammatory pathways and aggravate insulin resistance. Conversely, hepatic and intestinal cytokines, bile acids, hepatokines, and microbial metabolites may signal at vascular and neural interfaces, although direct causal evidence for brain effects in noncirrhotic MASLD remains limited. Lifestyle and cardiometabolic risk management remain foundational. Resmetirom and semaglutide have regulatory indications for selected adults with noncirrhotic MASH and moderate-to-advanced fibrosis, whereas microbiota-directed therapies and neuromodulation remain investigational. CONCLUSION: The liver-gut-brain axis is a useful integrative framework, but its component pathways have unequal evidentiary support. Longitudinal human studies using standardized hepatic, microbial, inflammatory, autonomic, and neurobehavioral outcomes are required before axis-based biomarkers or endotypes can guide routine care.
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The Gut Microbiota's Role in Neurological, Psychiatric, and Neurodevelopmental Disorders.
AIM: This article aims to explore the role of the human gut microbiota (GM) in the pathogenesis of neurological, psychiatric, and neurodevelopmental disorders, highlighting its influence on health and disease, and investigating potential therapeutic strategies targeting GM modulation. MATERIALS AND METHODS: A comprehensive analysis of the gut microbiota's composition and its interaction with the human body, particularly, its role in neurological and psychiatric conditions, is provided. The review discusses factors influencing GM composition, including birth mode, breastfeeding, diet, medications, and geography. Additionally, it examines the GM's functions, such as nutrient absorption, immune regulation, and pathogen defense, alongside its interactions with the nervous system through the gut-brain axis, neurotransmitters, and short-chain fatty acids (SCFAs). RESULTS: Alterations in the GM are linked to various disorders, including Parkinson's disease, multiple sclerosis, depression, schizophrenia, ADHD, and autism. The GM influences cognitive functions, stress responses, and mood regulation. Antibiotic use disrupts GM diversity, increasing the risk of metabolic disorders, obesity, and allergic diseases. Emerging therapies such as probiotics, prebiotics, and microbiota transplantation show promise in modulating the GM and alleviating symptoms of neurological and psychiatric conditions. CONCLUSIONS: The modulation of the GM represents a promising approach for personalized treatment strategies. Further research is needed to better understand the underlying mechanisms and to develop targeted therapies aimed at restoring GM balance for improved clinical outcomes.
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Microbe-Immune Crosstalk: Evidence That T Cells Influence the Development of the Brain Metabolome.
Cross-talk between the immune system and the brain is essential to neuronal development, neuronal excitability, neuroplasticity, and neurotransmission. Gut microbiota are essential to immune system development and immune function; hence, it is essential to consider more broadly the microbiota-immune-brain axis in neurodevelopment. The gut, brain, and microbial metabolomes obtained from C57Bl/6 and T-cell-deficient mice across four developmental timepoints (postnatal day 17, 24, 28, and 84) were studied by 1H NMR spectroscopy. 16S rRNA gene sequencing was performed on cecal and fecal samples. In the absence of T-cells, the developmental trajectory of the gut microbiota and of the host's metabolic profile was altered. The novel insights from this work include (1) the requirement of functional T-cells for the normal trajectory of microbiotal development and the metabolic maturation of the supra-organism, (2) the potential role for Muribaculaceae taxa in modulating the cecal availability of metabolites previously implicated with a role in the gut-brain axis in T-cell deficient mice, and (3) the impact of T-cell-deficiency on central levels of neuroactive metabolites.
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Can We Modulate Our Second Brain and Its Metabolites to Change Our Mood? A Systematic Review on Efficacy, Mechanisms, and Future Directions of "Psychobiotics".
Psychobiotics, live microorganisms that provide mental health by interacting with the gut microbiota, are emerging as a promising therapeutic option for psychiatric and neurodevelopmental disorders. Their effectiveness in addressing conditions such as depression, anxiety, insomnia, stress, autism spectrum disorder (ASD), and eating disorders were examined through a comprehensive analysis of existing studies up to the first half of 2024, based on data from reliable electronic databases. We found that psychobiotics can significantly reduce symptoms of various psychiatric disorders by influencing neurotransmitter levels, regulating the hypothalamic-pituitary-adrenal (HPA) axis, and improving gut barrier function through short-chain fatty acids (SCFAs) and other metabolites. However, several limitations were identified, including inconsistent study methodologies, small sample sizes, and a lack of data on long-term safety. Addressing these limitations through rigorous research is essential for establishing standardized protocols and fully confirming the therapeutic potential of psychobiotics. In conclusion, psychobiotics show great promise as complementary treatments for mental health conditions, but continued research is necessary to refine their application and integrate them into clinical practice effectively.
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Psychobiotic Properties of Lactiplantibacillus plantarum in Neurodegenerative Diseases.
Neurodegenerative disorders are the main cause of cognitive and physical disabilities, affect millions of people worldwide, and their incidence is on the rise. Emerging evidence pinpoints a disturbance of the communication of the gut-brain axis, and in particular to gut microbial dysbiosis, as one of the contributors to the pathogenesis of these diseases. In fact, dysbiosis has been associated with neuro-inflammatory processes, hyperactivation of the neuronal immune system, impaired cognitive functions, aging, depression, sleeping disorders, and anxiety. With the rapid advance in metagenomics, metabolomics, and big data analysis, together with a multidisciplinary approach, a new horizon has just emerged in the fields of translational neurodegenerative disease. In fact, recent studies focusing on taxonomic profiling and leaky gut in the pathogenesis of neurodegenerative disorders are not only shedding light on an overlooked field but are also creating opportunities for biomarker discovery and development of new therapeutic and adjuvant strategies to treat these disorders. Lactiplantibacillus plantarum (LBP) strains are emerging as promising psychobiotics for the treatment of these diseases. In fact, LBP strains are able to promote eubiosis, increase the enrichment of bacteria producing beneficial metabolites such as short-chain fatty acids, boost the production of neurotransmitters, and support the homeostasis of the gut-brain axis. In this review, we summarize the current knowledge on the role of the gut microbiota in the pathogenesis of neurodegenerative disorders with a particular focus on the benefits of LBP strains in Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, autism, anxiety, and depression.
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New Insights into the oral microbiota and host epigenetic changes in obsessive compulsive disorder and major depressive disorder: Focus on BDNF.
Obsessive-Compulsive Disorder (OCD) and Major Depressive Disorder (MDD) frequently co-occur, with depressive symptoms affecting OCD progression and vice versa. Identifying biomarkers is crucial for improving diagnosis and treatment. While the gut microbiota's role in psychiatric disorders is well-studied, this research focuses on alterations in the oral microbiota and their relationship with BDNF (Brain-Derived Neurotrophic Factor) DNA methylation in OCD and MDD patients compared to healthy controls. Our findings reveal significant changes in microbiota composition with OCD patients showing increased Actinobacteriota and Firmicutes abundances (p < 0.05; CTRL = n.24, OCD = n.29), while MDD patients exhibiting increased Actinobacteriota and Firmicutes, with reduced Bacteroidota and Proteobacteria abundances (p < 0.05; CTRL = n.24, MDD = n.20). These alterations, including potential post-streptococcal autoimmunity, highlight the microbiota's role in OCD and MDD pathophysiology. Selective changes in BDNF DNA methylation were observed in both disorders at CpG sites in exon I and IV, significantly reduced in OCD and MDD (p < 0.05; CTRL = n.24, OCD = n.29, MDD = n.20) and, following miRNome analysis, showed altered expression of BDNF-targeting microRNAs, with miR-16-5p and miR-29a-3p upregulated in OCD (p < 0.05; CTRL = n.24, OCD = n.17), and miR-29a-3p upregulated and miR-191-5p downregulated in MDD (p < 0.05; CTRL = n.24, MDD = n.16). These findings suggest disorder-specific microbiota and epigenetic profiles, positioning saliva as a non-invasive tool for biomarker identification. This research advances the understanding of microbial-epigenetic interactions in OCD and MDD, potentially guiding early diagnosis and targeted therapies.
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Lactobacillus acidophilus LA3 Suppresses Neuroinflammation via the Gut-Brain Axis.
The gut-brain axis represents a pivotal pathway through which gut microbiota influence neuroinflammation and neurological health. This study identifies Lactobacillus acidophilus LA3 as a potent probiotic strain capable of mitigating neuroinflammation. LA3 demonstrated superior efficacy in suppressing LPS-induced proinflammatory cytokines in BV-2 microglia. In an LPS-induced murine model, LA3 alleviated systemic and neuroinflammation, depressive-like behaviors, and cognitive impairment, while restoring blood-brain and gut-vascular barrier integrity. LA3 reversed gut microbiota dysbiosis, enriched short-chain fatty acid-producing bacteria, and promoted indole-3-acetic acid (IAA) levels in colonic contents and brain. The anti-inflammatory effect of LA3 was AHR-dependent, as confirmed by an AHR inhibitor in BV-2 cells. Notably, both LA3 fermentation supernatant and exogenous IAA (at the same dose as detected in the supernatant) recapitulated key aspects of LA3's effects. Collectively, L. acidophilus LA3 represents a promising next-generation probiotic targeting the gut-brain axis, with IAA serving as an important effector in neuroinflammation resolution.